
Jiayu Lv
Postdoctoral Scholar, Cardiovascular Institute
All Publications
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The role of circulating cytokines in heart failure: a bidirectional, two-sample Mendelian randomization study.
Frontiers in cardiovascular medicine
2024; 11: 1332015
Abstract
Cytokines play a pivotal role in the progression of heart failure (HF) by modulating inflammatory responses, promoting vasoconstriction, and facilitating endothelial injury. However, it is now difficult to distinguish the causal relationship between HF and cytokines in observational studies. Mendelian randomization (MR) analyses of cytokines probably could enhance our comprehension to the underlying biological processes of HF.This study was to explore the correlation between 41 cytokines with HF at the genetic level by MR analysis. We selected a HF dataset from the Heart Failure Molecular Epidemiology for Therapeutic Targets (HERMES) 2018 and a cytokine dataset from a meta-analysis of cytokine levels in Finns. Two-sample, bidirectional MR analyses were performed using Inverse Variance Weighted (IVW), Weighted Median and MR- egger, and the results were tested for heterogeneity and pleiotropy, followed by sensitivity analysis.Genetic prediction of high levels of circulating Macrophage inflammatory pro-tein-1β(MIP-1β) (P = 0.0389), Interferon gamma induced protein 10(IP-10) (P = 0.0029), and Regu-lated on activation, normal T cell expressed and secreted(RANTES) (P = 0.0120) expression was associated with an elevated risk of HF. HF was associated with the increased levels of circulating Interleukin-2 receptor, alpha subunit(IL-2ra) (P = 0.0296), Beta nerve growth fac-tor(β-NGF) (P = 0.0446), Interleukin-17(IL-17) (P = 0.0360), Basic fibroblast growth factor(FGF-basic) (P = 0.0220), Platelet derived growth factor BB(PDGF-BB) (P = 0.0466), and Interferon-gamma(IFN-γ) (P = 0.0222); and with decreased levels of Eotaxin (P = 0.0133). The heterogeneity and pleiotropy of the cytokines were acceptable, except for minor heterogeneity of FGF-basic and IL-17.These findings provide compelling evidence for a genetically predictive relationship between cytokines and HF, emphasizing a great potential of targeted modulation of cytokines in slowing the progression of HF. This study draws further conclusions at the genetic level, providing a basis for future large-scale clinical trials.
View details for DOI 10.3389/fcvm.2024.1332015
View details for PubMedID 39502198
View details for PubMedCentralID PMC11534875
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Exploring the inflammation-related mechanisms of Lingguizhugan decoction on right ventricular remodeling secondary to pulmonary arterial hypertension based on integrated strategy using UPLC-HRMS, systems biology approach, and experimental validation.
Phytomedicine : international journal of phytotherapy and phytopharmacology
2024; 132: 155879
Abstract
Pulmonary arterial hypertension (PAH) and the consequent right heart dysfunction persist with high morbidity and mortality, and the mechanisms and pharmacologic interventions for chronic right-sided heart failure (RHF) have not been adequately investigated. Research has shown that prolonged inflammation is critical in precipitating the progression of PAH-associated right heart pathology. Some research demonstrated that Lingguizhugan decoction (LGZGD), as a classical Chinese medicine formula, had beneficial effects in alleviating PAH and RHF, while its underlying mechanisms involved are not fully elucidated.Based on that, this study aims to investigate the effects and underlying mechanisms of LGZGD on PAH-induced RHF.In this study, we identified the serum constituents and deciphered the potential anti-inflammatory mechanism and crucial components of LGZGD using combined approaches of UPLC-HRMS, transcriptomic analysis, and molecular docking techniques. Finally, we used in vivo experiments to verify the expression of key targets in the monocrotaline (MCT)-induced RHF model and the intervene effect of LGZGD.Integrated strategies based on UPLC-HRMS and systems biology approach combined with in vivo experimental validation showed that LGZGD could improve right heart fibrosis and dysfunction via regulating diverse inflammatory signaling pathways and the activity of immune cells, including chemokine family CCL2, CXCR4, leukocyte integrins family ITGAL, ITGB2, and M2 macrophage infiltration, as well as lipid peroxidation-associated HMOX1, NOX4, and 4-HNE.The present research demonstrated for the first time that LGZGD might improve PAH-induced RHF through multiple anti-inflammatory signaling and inhibition of ferroptosis, which could provide certain directions for future research in related fields.
View details for DOI 10.1016/j.phymed.2024.155879
View details for PubMedID 39032277
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Mechanism of Zhenwu Decoction modulating TLR4/NF-κB/HIF-1α loop through miR-451 to delay renal fibrosis in type 2 CRS.
Phytomedicine : international journal of phytotherapy and phytopharmacology
2024; 132: 155632
Abstract
Type 2 cardiorenal syndrome (CRS) is a progressive renal insufficiency in patients with chronic heart failure, but its pathophysiology is still unclear. The Chinese medicine Zhenwu Decoction plays an important role in the prevention and treatment of 2-CRS, however, its mechanism of action remains unknown.The aim of this study was to investigate whether the ameliorative effect of ZWD on 2-CRS renal fibrosis is related to the modulation of miR-451 expression and thus mediating the TLR4/NF-κB/HIF-1α loop.A type 2 CRS rat model was constructed using ligation of the left anterior descending branch of the coronary artery + 3/4 nephrectomy, and randomly divided into Control, Sham, Model, Captopril, ZWD-L, ZWD-M and ZWD-H groups.After 4 weeks of ZWD intervention, its effects on cardiac and renal functions of type 2 CRS rats were observed by hematuria and cardiac ultrasonography. Changes in kidney tissue morphology were observed by HE, Masson and PASM staining. The protein and mRNA expression of TLR4, NF-κB, HIF-1α and IκBα in kidney tissues were detected by immunohistochemistry and qPCR. Immunofluorescence was used to detect the protein expression of NF-κB and HIF-1α in renal tissues. Western blot and qPCR were used to detect the protein expression of MCP-1, ICAM-1, IL-1β, IL-6, TGF-β, α-SMA, FN, Smad2, Smad3, and E-cadherin in renal tissues. PCR was used to detect the protein expression of miR-451mRNA expression level in kidney tissues.In this study, we found that ZWD was able to reduce the expression of Scr, BUN, NT-proBNP, and 24-hour quantitative urine protein, elevate LVEF, FS, CO, and reduce the level of LVIDS in type 2 CRS rats, as well as attenuate renal interstitial fibrosis and improve tubular swelling. In addition, Zhenwu Decoction up-regulated the expression of miR-451 in renal tissues and inhibited the expression of TLR4, NF-κB, and HIF-1α proteins and genes, which in turn inhibited the expression of inflammatory factors and fibrosis-related factors.ZWD was able to up-regulate the expression of miR-451 in renal tissues, inhibit the TLR4/NF-κB/HIF-1α response loop, and then inhibit the expression of inflammatory factors and fibrosis-related factors, improve renal fibrosis, and delay the pathological process of type 2 CRS.
View details for DOI 10.1016/j.phymed.2024.155632
View details for PubMedID 38851985
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Global research trends and emerging opportunities for integrin adhesion complexes in cardiac repair: a scientometric analysis.
Frontiers in cardiovascular medicine
2024; 11: 1308763
Abstract
Cardiac regenerative medicine has gained significant attention in recent years, and integrins are known to play a critical role in mediating cardiac development and repair, especially after an injury from the myocardial infarction (MI). Given the extensive research history and interdisciplinary nature of this field, a quantitative retrospective analysis and visualization of related topics is necessary.We performed a scientometric analysis of published papers on cardiac integrin adhesion complexes (IACs), including analysis of annual publications, disciplinary evolution, keyword co-occurrence, and literature co-citation.A total of 2,664 publications were finally included in the past 20 years. The United States is the largest contributor to the study and is leading this area of research globally. The journal Circulation Research attracts the largest number of high-quality publications. The study of IACs in cardiac repair/regenerative therapies involves multiple disciplines, particularly in materials science and developmental biology. Keywords of research frontiers were represented by Tenasin-C (2019-2023) and inflammation (2020-2023).Integrins are topics with ongoing enthusiasm in biological development and tissue regeneration. The rapidly emerging role of matricellular proteins and non-protein components of the extracellular matrix (ECM) in regulating matrix structure and function may be a further breakthrough point in the future; the emerging role of IACs and their downstream molecular signaling in cardiac repair are also of great interest, such as induction of cardiac proliferation, differentiation, maturation, and metabolism, fibroblast activation, and inflammatory modulation.
View details for DOI 10.3389/fcvm.2024.1308763
View details for PubMedID 38699584
View details for PubMedCentralID PMC11063371
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Qi-Po-Sheng-Mai granule ameliorates Ach-CaCl2 -induced atrial fibrillation by regulating calcium homeostasis in cardiomyocytes.
Phytomedicine : international journal of phytotherapy and phytopharmacology
2023; 119: 155017
Abstract
Atrial fibrillation (AF) is one of the most common arrhythmias encountered in clinical settings. Currently, the pathophysiology of AF remains unclear, which severely limits the effectiveness and safety of medical therapies. The Chinese herbal formula Qi-Po-Sheng-Mai Granule (QPSM) has been widely used in China to treat AF. However, its pharmacological and molecular mechanisms remain unknown.The purpose of this study was to investigate the molecular mechanisms and potential targets of QPSM for AF.The AF model was induced by Ach (66 μg/ml) and CaCl2 (10 mg/kg), and the dose of 0.1 ml/100 g was injected into the tail vein for 5 weeks. QPSM was administered daily at doses of 4.42 and 8.84 g/kg, and amiodarone (0.18 g/kg) was used as the positive control. The effect of QPSM on AF was assessed by electrocardiogram, echocardiography, and histopathological analysis. Then, we employed network pharmacology with single nucleus RNA sequencing (snRNA-Seq) to investigate the molecular mechanisms and potential targets of QPSM for AF. Furthermore, high performance liquid chromatography (HPLC) method was used for component analysis of QPSM, and molecular docking was used to verify the potential targets. Using the IonOptix single cell contraction and ion synchronization test equipment, single myocyte length and calcium ion variations were observed in real time. The expression levels of calcium Transporter-related proteins were detected by western blot and immunohistochemistry.Based on an Ach-CaCl2-induced AF model, we found that QPSM treatment significantly reduced atrial electrical remodeling-related markers, such as AF inducibility and duration, and attenuated atrial dilation and fibrosis. Network pharmacology identified 52 active ingredients and 119 potential targets for QPSM in the treatment of AF, and 45 Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways were enriched, among which calcium pathway had the greatest impact. Using single nucleus sequencing (snRNA-seq), we identified cardiomyocytes as the most differentially expressed in response to drug treatment, with nine differentially expressed genes enriched in calcium signaling pathways. High performance liquid chromatography and molecular docking confirmed that the core components of QPSM strongly bind to the key factors in the calcium signaling pathway. Additional experiments have shown that QPSM increases calcium transients (CaT) and contractility in the individual cardiomyocyte. This was accomplished by increasing the expression of CACNA1C and SERCA2a and decreasing the expression of CAMK2B and NCX1.The present study has systematically elucidated the role of QPSM in maintaining calcium homeostasis in cardiomyocytes through the regulation of calcium transporters, which could lead to new drug development ideas for AF.
View details for DOI 10.1016/j.phymed.2023.155017
View details for PubMedID 37597360
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Renal fibrosis in type 2 cardiorenal syndrome: An update on mechanisms and therapeutic opportunities.
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
2023; 164: 114901
Abstract
Cardiorenal syndrome (CRS) is a state of coexisting heart failure and renal insufficiency in which acute or chronic dysfunction of the heart or kidney lead to acute or chronic dysfunction of the other organ.It was found that renal fibrosis is an important pathological process in the progression of type 2 CRS to end-stage renal disease, and progressive renal impairment accelerates the deterioration of cardiac function and significantly increases the hospitalization and mortality rates of patients. Previous studies have found that Hemodynamic Aiteration, RAAS Overactivation, SNS Dysfunction, Endothelial Dysfunction and Imbalance of natriuretic peptide system contribute to the development of renal disease in the decompensated phase of heart failure, but the exact mechanisms is not clear. Therefore, in this review, we focus on the molecular pathways involved in the development of renal fibrosis due to heart failure and identify the canonical and non-canonical TGF-β signaling pathways and hypoxia-sensing pathways, oxidative stress, endoplasmic reticulum stress, pro-inflammatory cytokines and chemokines as important triggers and regulators of fibrosis development, and summarize the therapeutic approaches for the above signaling pathways, including SB-525334 Sfrp1, DKK1, IMC, rosarostat, 4-PBA, etc. In addition, some potential natural drugs for this disease are also summarized, including SQD4S2, Wogonin, Astragaloside, etc.
View details for DOI 10.1016/j.biopha.2023.114901
View details for PubMedID 37224755
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Frontier and Hotspot Evolution in Cardiorenal Syndrome: A Bibliometric Analysis From 2003 to 2022.
Current problems in cardiology
2023; 48 (8): 101238
Abstract
In the last 20 years, the cardiorenal syndrome (CRS) field has received growing attention. There have been innovations in cardiorenal interaction patterns, biological markers and management of CRS, and even significant changes in its concept and the paradigm of CRS pathophysiology, which considerably increases the difficulties in understanding and in-depth study of this field. However, few study summarized the development process of CRS and critical issues. This review focuses on topical evolutions and emerging trends in CRS pathophysiology, diagnostic pathways, and treatment strategies. A quantitative retrospective analysis, visual review, and evaluation of 1452 articles published in the domain of CRS from 2003 to 2022 was conducted using a bibliometric analysis based on the classic CiteSpace and VOSviewer software rather than a general review, aiming to provide reasonable ideas and directions for future research on CRS.
View details for DOI 10.1016/j.cpcardiol.2022.101238
View details for PubMedID 35500729
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Opportunities and Challenges in Cardio-Oncology: A Bibliometric Analysis From 2010 to 2022.
Current problems in cardiology
2023; 48 (8): 101227
Abstract
Cardio-oncology has grown rapidly worldwide as an emerging interdisciplinary discipline over the past decade. In the present bibliometric review, we employed VOSviewer and Citespace software to describe the literature landscape concerning cardio-oncology from 2010 to 2022. As a result, a total of 1,194 relevant publications were identified in the Web of Science database with an increasing trend. The United States dominated the field during the research period, and Italy, England and Canada had emerged as significant contributors to the study. Ky. Bonnie, Herrmann. Joerg and Fradley. Michael G were the most productive researchers. JACC: CardioOncology was the journal dedicated to the discipline of cardio-oncology and had published the greatest number of papers. Vascular disease and atrial fibrillation have attracted much attention as the main cardiovascular burden. Immune checkpoint inhibitor-specific cardiovascular toxicity, biomarkers and imaging examination together with the prevention of cardio-oncology are potential research hotspots. Notably, basic research is lagging behind, for which more researches are needed to fill the gap. In conclusion, bibliometric analysis provided valuable information for the development of cardio-oncology, which is full of opportunities and challenges.
View details for DOI 10.1016/j.cpcardiol.2022.101227
View details for PubMedID 35500730
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Effects of garlic supplementation on components of metabolic syndrome: a systematic review, meta-analysis, and meta-regression of randomized controlled trials.
BMC complementary medicine and therapies
2023; 23 (1): 260
Abstract
Garlic (Allium sativum), the underground bulb of the Allium genus, has been consumed on Earth for thousands of years. Many clinical trials of garlic supplementation on components of metabolic syndrome (MetS) have emerged in recent years, but there is no consensus on the effect. This meta-analysis aimed at systematically evaluating the effect of garlic supplementation on components of MetS.In this meta-analysis, we searched Pubmed, Embase, Cochrane, Medline, Web of Science databases, and clinical trials online sites from inception to November 1, 2022, with language restrictions to English. We engaged participants > 18 years and eligible for the clinical diagnosis of MetS or those with metabolic disorders and garlic was the only intervention. Outcomes included waist circumference, and body mass index, triglycerides, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, blood pressure, and fasting blood glucose. Meta-regression and subgroup analyses were conducted based on six covariates (total sample size, the mean age, the mean dose, the duration of intervention, the oral form of garlic, and the dietary intervention).Results from 19 RCTs were included engaging 999 participants. Compared to placebo, garlic significantly reduced TG [SMD (95%CI) = -0.66 (-1.23, -0.09)], TC [SMD (95%CI) = -0.43 (-0.86, -0.01)], LDL [SMD (95%CI) = -0.44(-0.88, -0.01)], DBP [SMD (95%CI) = -1.33 (-2.14, -0.53)], BMI [SMD (95%CI) = -1.10(-1.90, -0.20)], and WC [SMD (95%CI) = -0.78(-1.09, -0.47)]. Meta-regression showed age and sample size are potential effect modifiers.According to the results of meta-analysis, the modulatory effect of garlic on some MetS components is evident. More high-quality, large-scale RCTs are needed to confirm iat based on the high heterogeneity and potential publication bias of the current data.https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=373228 , ID: CRD42022373228.
View details for DOI 10.1186/s12906-023-04038-0
View details for PubMedID 37481521
View details for PubMedCentralID PMC10362699
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Research trends and hotspots evolution of cardiac amyloidosis: a bibliometric analysis from 2000 to 2022.
European journal of medical research
2023; 28 (1): 89
Abstract
In the new century, cardiac amyloidosis has received more attention from many countries and institutions, leading to innovations in the essence of the pathology, biological markers, noninvasive tests, and staging diagnoses and treatments for this disease. However, few reviews have summarized the research trends and hotspots in cardiac amyloidosis. Bibliometrics analysis is a statistically based approach to research that visualizes the contributions of academic institutions and changes in research hotspots. Therefore, in this paper, we used Citespace and VOSviewer software to conduct co-occurrence analysis and collaborative network analysis on the countries, institutions, and authors in the articles related to cardiac amyloidosis since the new century. And further find out burst keywords and references to obtain the research history, disciplinary development, and new hotspots and topics.
View details for DOI 10.1186/s40001-023-01026-5
View details for PubMedID 36805827
View details for PubMedCentralID PMC9940355
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Trends in research on sick sinus syndrome: A bibliometric analysis from 2000 to 2022.
Frontiers in cardiovascular medicine
2022; 9: 991503
Abstract
Sick sinus syndrome (SSS) is a refractory arrhythmia disease caused by the pathological changes of sinoatrial node and its adjacent tissues. 2,251 publications related to SSS were retrieved from Web of Science database from 2000 to 2022 and analyzed by using VOS viewer and CiteSpace software. The results showed the United States dominated the field, followed by Japan, Germany, and China. SSS was closely related to risk factors such as atrial fibrillation and aging. Sick sinus syndrome, atrial fibrillation and sinus node dysfunction were the top three keywords that had the strongest correlation with the study. Pacemaker implantation, differentiation and mutation are research hotspots currently. Clinical studies on SSS found that sick sinus syndrome, atrial fibrillation, and pacemakers were the top three keywords that had the largest nodes and the highest frequency. In the field of basic applied research and basic research, atrial fibrillation and pacemaker cells were the focus of research. In conclusion, bibliometric analysis provided valuable information for the prevention, treatment and future research trends of SSS.
View details for DOI 10.3389/fcvm.2022.991503
View details for PubMedID 36440047
View details for PubMedCentralID PMC9681915
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Skeletal muscle mitochondrial remodeling in heart failure: An update on mechanisms and therapeutic opportunities.
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
2022; 155: 113833
Abstract
Patients with heart failure (HF) usually present with skeletal muscle diseases of varying severity, ranging from early fatigue on exercise to sarcopenia, sarcopenic obesity or cachexia, and frailty, which are significant predictors of HF prognosis. Abnormal mitochondrial metabolism has been identified as one of the earliest signs of skeletal muscle injury in HF and is associated with pathological alterations in muscle, manifested as muscle wasting, myocyte atrophy and apoptosis, fiber type shift, impaired contractile coupling, and muscle fat infiltration. In this review, we update the evidence for skeletal muscle mitochondrial remodeling in HF patients or animal models, including the impairments in mitochondrial ultrastructure, oxidative metabolism, electron transport chain (ETC), phosphorylation apparatus, phosphotransfer system, and quality control. We also focus on molecular regulatory mechanisms upstream of mitochondria, including circulating factors (e.g., RAAS, TNF-α IL-6, IGF-1, GH, ghrelin, adiponectin, NO) and molecular signals within myocytes (e.g., PGC-1α, PPARs, AMPK, SIRT1/3, ROS, and MuRF1). Besides the therapies targeting the signaling pathways mentioned above, such as AdipoRon and elamipretide, we further summarize other potential pharmacological approaches like inhibitors of sodium-glucose cotransporter 2 (SGLT2) and dipeptidyl peptidase-4 (DPP-4), as well as some natural products, which may have the beneficial effects on improving the skeletal muscle mitochondrial function of HF. Targeting myocyte mitochondrial biogenesis, oxidative metabolism, oxidative phosphorylation, and reduction of oxidative stress injury are promising future opportunities for the prevention and management of skeletal muscle myopathy in HF.
View details for DOI 10.1016/j.biopha.2022.113833
View details for PubMedID 36271583
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Roles and mechanisms of quercetin on cardiac arrhythmia: A review.
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
2022; 153: 113447
Abstract
Cardiac arrhythmia is one of the most prevalent cardiovascular diseases worldwide, which can occur alone or be triggered by other diseases, and it can be fatal in severe cases. Recently, Traditional Chinese Medicine has drawn the world's attention to its effective treatment. As a natural polyhydroxy flavonoid mainly isolated from a variety of plants and foods, quercetin is used for the treatment of cardiovascular disease, cancer, autoimmune diseases, and neurological disorders. A growing number of in vitro experiments and in vivo animal studies have shown that quercetin significantly inhibits mitochondrial oxidative stress, cardiac fibrosis, inflammatory responses, and apoptosis, regulates autophagic responses, improves ischemia/reperfusion injury in cardiomyocytes, and regulates gut microbiota, thereby attenuating or preventing structural and electrical remodeling in the cardiac. Based on these mechanisms, our review provides a systematic overview of the pharmacological actions and molecular targets of quercetin in cardiac arrhythmia caused by multiple etiologies, aiming to provide novel insights and therapeutic strategies to prevent or ameliorate arrhythmia.
View details for DOI 10.1016/j.biopha.2022.113447
View details for PubMedID 36076562
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Tongxinluo capsule as supplementation and cardiovascular endpoint events in patients with coronary heart disease: A systematic review and meta-analysis of randomized, double-blind, placebo-controlled trials.
Journal of ethnopharmacology
2022; 289: 115033
Abstract
Tongxinluo Capsule(TXLC) is a well-known traditional Chinese medicine prescription with effects of tonifying Qi and activating blood based on the Chinese herbal medicine theory that has been recommended as routine adjuvant treatment in patients with coronary heart disease (CHD) in China.This meta-analysis aimed to evaluate the efficacy and safety of TXLC as supplementation in the prevention of adverse cardiovascular events in patients with CHD.We performed a literature search in Pubmed, Cochrane Library, China National Knowledge Infrastructure (CNKI), Chinese Scientific Journals Database (VIP), Wan Fang Database, and Chinese Biomedical Database (CBM) from their inceptions to March 2020. Only randomized controlled trials (RCTs) that assessed supplementation with TXLC or placebo and with adverse cardiovascular outcomes, were included in this meta-analysis. Primary end points were myocardial infarction (MI), target vessel revascularization (TVR) or in-stent restenosis (ISR), and cardiovascular death. Secondary end points included cerebrovascular accidents, heart failure (HF), and unscheduled readmission for cardiovascular diseases (CVDs). Adverse drug events were also evaluated. Trial sequential analysis (TSA) was conducted to reduce random errors introduced by possible insufficient sample size.Eleven RCTs involving 1505 patients were analyzed. The mean(SD) age of included patients were 59.03(9.7) years. Treatment duration varied from 2 months to 12 months. Compared with placebo, TXLC supplementation showed significant effects on reducing the risk of MI (RR = 0.44, [95% CI, 0.24-0.80]), TVR or ISR (RR = 0.43, [95% CI, 0.31-0.58]), cerebrovascular accidents(RR = 0.17, [95% CI, 0.06-0.46]), HF (RR = 0.41, [95% CI, 0.21-0.79]), and unscheduled readmission for CVDs (RR = 0.72, [95% CI], P = 0.04), but did not have associations with incidence of cardiovascular death (RR = 0.53, [95% CI, 0.15-1.91]). Subgroups of trials with 2-month (MI: RR = 0.44, [95% CI, 0.13-1.53]; cardiovascular death: RR = 0.30, [95% CI, 0.01-7.67]; cerebrovascular accidents: RR = 0.04, [95% CI, 0.01-0.26]; unscheduled readmission for CVDs: RR = 0.43, [95% CI, 0.20-0.94]) and 12-month (MI: RR = 0.42, [95% CI, 0.20-0.89]; TVR or ISR: RR = 0.42, [95% CI, 0.31-0.58]; HF: RR = 0.34, [95% CI, 0.14-0.78]; unscheduled readmission for CVDs: RR = 0.85, [95% CI, 0.59-1.22]) intervention period were analyzed. The adverse drug reactions were mild with no significant difference between TXLC and placebo.This meta-analysis indicated that TXLC supplementation had beneficial effects on the prevention of cardiovascular adverse events, especially in TVR or ISR after coronary revascularization and may possibly lower the incidence of first or recurrent MI and HF within 12 months in patients with CHD, while insufficient sample size implied that these results lacked certain stability. And the effects of TXLC on cardiovascular mortality, cerebrovascular events, and unscheduled readmission for CVDs could not be confirmed due to insufficient cases. Clinical trials with large-sample sizes and extended follow-up time are of interest in the future researches.
View details for DOI 10.1016/j.jep.2022.115033
View details for PubMedID 35091010
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The Application of Angiotensin Receptor Neprilysin Inhibitor in Cardiovascular Diseases: A Bibliometric Review From 2000 to 2022.
Frontiers in cardiovascular medicine
2022; 9: 899235
Abstract
Cardiovascular disease (CVD) has become a huge challenge for the global public health system due to its high morbidity, mortality and severe economic burden. In recent years, angiotensin receptor neprilysin inhibitor (ARNI), a new class of drugs, has shown good therapeutic effects on CVD patients in several clinical studies, reducing the morbidity and mortality of CVD patients. In this study, we retrieved publications on ARNI research in the cardiovascular field from the Web of Science core collection and analyzed the annual output, spatial and temporal distribution, institutions and authors, core journals, keywords and co-cited literature based on CiteSpace. As a result, 604 publications were retrieved, and the number of annual publications generally increased year by year, with the largest number of articles. The analysis of the co-occurrence of output countries and authors showed that a few developed countries such as the United States, Canada, and United Kingdom are the most active in this field, forming academic groups represented by John Joseph Valentine McMurray and Scott D. Solomon, and New England Journal of Medicine, Cirulation, and Journal of the American College of Cardiology are the most popular journals in the field, with research hotspots focused on ARNI in the treatment of total ejection fraction heart failure, hypertension and its target organ damage, with the potential for future benefit throughout the cardiovascular event chain as research progresses. This study reveals the prospective application of ARNI in the cardiovascular field and the research hotspots, providing broader and deeper guidance for its use in the clinic, which is beneficial to improve the treatment and prognosis of CVD patients.
View details for DOI 10.3389/fcvm.2022.899235
View details for PubMedID 35600466
View details for PubMedCentralID PMC9114353
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Bibliometric Analysis of Birt-Hogg-Dubé Syndrome From 2001 to 2021.
Frontiers in medicine
2022; 9: 857127
Abstract
Birt-Hogg-Dubé syndrome (BHD) is a rare autosomal dominant inherited disorder caused by germline mutations in folliculin (FLCN). Despite our significantly evolved understanding of BHD over the past decades, no bibliometric analyses have been conducted in this field. This study aimed to analyze and visualize the characteristics of publication outputs, the research hotspots, and scientific frontiers about BHD using bibliometric analysis.All relevant literature on BHD was culled from the Web of Science Core Collection (WoSCC) database. Valid data were extracted from the articles and visually analyzed using CiteSpace and VOSviewer.A total of 751 qualifying papers were included. Publication outputs concerning BHD increased over time. The dominant position of the United States and Japan in BHD research field was evident. National Cancer Institute (the USA) and Yokohama City University (Japan) were the two most productive organizations. W. Marston Linehan exerted a considerable publication impact and had made the most remarkable contributions in the field of BHD. Plos One was the journal with the highest publication outputs, and half of the top 10 journals and co-cited journals belonged to Q1 or Q2. Keyword citation bursts revealed that management, tumor suppressor, flcn gene, spectrum, diagnosis, risk, computed tomography were the emerging research hotspots.Research on BHD is prosperous. International cooperation between countries and organizations is also expected to deepen and strengthen in the future. Our results indicated that FLCN-associated pathways involved in the pathogenesis of BHD, specific options for early diagnosis, and molecular-targeting therapies will remain research hotspots in the future.
View details for DOI 10.3389/fmed.2022.857127
View details for PubMedID 35479937
View details for PubMedCentralID PMC9035795
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Role of puerarin in pathological cardiac remodeling: A review.
Pharmacological research
2022; 178: 106152
Abstract
Pathological cardiac remodeling normally involves changes in structure, function, and energy metabolism of the heart induced by cardiac injury or load, terminally leading to heart failure. Cardiac remodeling plays an essential role in the progression of cardiovascular disease, thus increasingly identified as an important therapeutic target for heart failure of all pathogenesis. Puerarin, as a natural isoflavone mainly from Pueraria lobata (Willd.)Ohwi, has been developed as injections, eye drops, microemulsions, etc., and is widely used in the clinical treatment of cardiovascular diseases in eastern Asia countries. In recent years, a growing number of studies have shown that puerarin significantly inhibits myocardial hypertrophic growth, myocyte death, fetal gene expression, fibroblast proliferation and activation, improves energy metabolism, promotes post-infarction angiogenesis, and suppresses inflammation and oxidative stress, consequently attenuating or preventing cardiac remodeling in response to multiple stimuli ( e.g., pressure overload, MIRI, MI, Iso, and Ang II stimulation). This review summarized the roles and underlying molecular mechanisms of puerarin in cardiac remodeling induced by diverse etiologies, aiming to help develop novel therapeutic strategies to prevent or reverse pathological ventricular remodeling.
View details for DOI 10.1016/j.phrs.2022.106152
View details for PubMedID 35248700
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Mitochondrial Dysfunction: An Emerging Link in the Pathophysiology of Cardiorenal Syndrome.
Frontiers in cardiovascular medicine
2022; 9: 837270
Abstract
The crosstalk between the heart and kidney is carried out through various bidirectional pathways. Cardiorenal syndrome (CRS) is a pathological condition in which acute or chronic dysfunction in the heart or kidneys induces acute or chronic dysfunction of the other organ. Complex hemodynamic factors and biochemical and hormonal pathways contribute to the development of CRS. In addition to playing a critical role in generating metabolic energy in eukaryotic cells and serving as signaling hubs during several vital processes, mitochondria rapidly sense and respond to a wide range of stress stimuli in the external environment. Impaired adaptive responses ultimately lead to mitochondrial dysfunction, inducing cell death and tissue damage. Subsequently, these changes result in organ failure and trigger a vicious cycle. In vitro and animal studies have identified an important role of mitochondrial dysfunction in heart failure (HF) and chronic kidney disease (CKD). Maintaining mitochondrial homeostasis may be a promising therapeutic strategy to interrupt the vicious cycle between HF and acute kidney injury (AKI)/CKD. In this review, we hypothesize that mitochondrial dysfunction may also play a central role in the development and progression of CRS. We first focus on the role of mitochondrial dysfunction in the pathophysiology of HF and AKI/CKD, then discuss the current research evidence supporting that mitochondrial dysfunction is involved in various types of CRS.
View details for DOI 10.3389/fcvm.2022.837270
View details for PubMedID 35282359
View details for PubMedCentralID PMC8914047