All Publications
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Metabolic changes in kidney stone disease.
Frontiers in immunology
2023; 14: 1142207
Abstract
Kidney stone disease (KSD) is one of the earliest medical diseases known, but the mechanism of its formation and metabolic changes remain unclear. The formation of kidney stones is a extensive and complicated process, which is regulated by metabolic changes in various substances. In this manuscript, we summarized the progress of research on metabolic changes in kidney stone disease and discuss the valuable role of some new potential targets. We reviewed the influence of metabolism of some common substances on stone formation, such as the regulation of oxalate, the release of reactive oxygen species (ROS), macrophage polarization, the levels of hormones, and the alternation of other substances. New insights into changes in substance metabolism changes in kidney stone disease, as well as emerging research techniques, will provide new directions in the treatment of stones. Reviewing the great progress that has been made in this field will help to improve the understanding by urologists, nephrologists, and health care providers of the metabolic changes in kidney stone disease, and contribute to explore new metabolic targets for clinical therapy.
View details for DOI 10.3389/fimmu.2023.1142207
View details for PubMedID 37228601
View details for PubMedCentralID PMC10203412
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Metformin suppresses calcium oxalate crystal-induced kidney injury by promoting Sirt1 and M2 macrophage-mediated anti-inflammatory activation.
Signal transduction and targeted therapy
2023; 8 (1): 38
View details for DOI 10.1038/s41392-022-01232-3
View details for PubMedID 36702833
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The influencing factors of infectious complications after percutaneous nephrolithotomy: a systematic review and meta-analysis.
Urolithiasis
2022; 51 (1): 17
Abstract
Infection is the most common complications of percutaneous nephrolithotomy (PCNL) in treating urinary calculi. However, the risk factors for developing infectious complications after surgery have not been clarified, and the predictive value of some factors is controversial. This study aimed to assess the risk factors for postoperative infectious complications of PCNL. We performed a systematic search of PubMed, Web of Science, Cochrane Library, and EMBASE to obtain studies reporting risk factors for postoperative infection complications after PCNL. In this review, demographic factors, laboratory test factors, and perioperative factors were evaluated. The odds ratio (OR) or mean difference (MD) with a 95% confidence interval (CI) was calculated to assess the risk factors. A total of 18 studies were included, with a total of 7161 study patients with a mean age of 46.4 to 55.5years and an incidence of infectious complications after PCNL ranging from 2.4% to 40.4%. Twelve factors were identified as independent risk factors for post-PCNL infection complications (P<0.05), female (OR=1.60, 95% CI 1.23-2.07), positive urine culture (UC) (OR=3.16, 95% CI 2.11-4.74), positive renal pelvis urine culture (RPUC) (OR=5.81, 95% CI 1.75-19.32), positive stone culture (SC) (OR=5.11, 95% CI 1.46-17.89), positive urine leukocyte (OR=3.61, 95% CI 2.45-5.34), infected stones (OR=7.00, 95% CI 1.27-38.55), elevated blood leukocyte (MD=0.71, 95% CI 0.31-1.10), elevated neutrophil-to-lymphocyte ratio (NLR) (MD=0.55, 95% CI 0.43-0.66), preoperative stenting (OR=1.55, 95% CI 1.10-2.20), multiple puncture access (OR=2.58, 95% CI 1.75-3.82), prolonged operative time (MD=10 20, 95% CI 4.80-15.60), and postoperative residual stone (OR=1.56, 95% CI 1.24-1.98). Female, UC positivity, RPUC positivity, SC positivity, urine leukocyte positivity, infected stones, elevated peripheral blood leukocytes, elevated NLR, preoperative stent implantation, multiple puncture channels, prolonged operation time, and postoperative residual stones were identified as independent risk factors for infection complications after PCNL.
View details for DOI 10.1007/s00240-022-01376-5
View details for PubMedID 36515726
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NEAT1 regulates CaOx crystal-induced renal tubular oxidative injury via miR-130/IRF1.
Antioxidants & redox signaling
2022
Abstract
Abstract： Aims: Calcium oxalate (CaOx) crystal deposition induces damage to the renal tubular epithelium, increases epithelial adhesion, and contributes to CaOx nephrocalcinosis. The long noncoding RNA (lncRNA) NEAT1 is thought to be involved in this process. In this study, we aimed to investigate the mechanism by which NEAT1 regulates renal tubular epithelium in response to inflammatory and oxidative injury triggered by CaOx crystals. Results: As CaOx crystals were deposited in mouse kidney tissue, the expression of NEAT1 was significantly elevated and positively correlated with IRF1, TLR4, and NF-κB. NEAT1 targets and inhibits miR-130a-3p as a competitor to endogenous RNA (ceRNA). miR-130 binds to and exerts inhibitory effects on the 3'UTR of IRF1. After transfected with silence-NEAT1, IRF1, TLR4 and NF-κB were also variously inhibited, and oxidative damage in renal calcinosis was subsequently attenuated. When we simultaneously inhibited NEAT1 and miR-130, renal tubular injury was exacerbated. Innovation and Conclusion: We found that the lncRNA NEAT1 can enhance IRF1 signaling through targeted repression of miR-130a-3p and activate TLR4/NF-κB pathways to promote oxidative damage during CaOx crystal deposition. This provides an explanation for the tubular epithelial damage caused by CaOx crystals and offers new ideas and drug targets for the prevention and treatment of CaOx nephrocalcinosis.
View details for DOI 10.1089/ars.2022.0008
View details for PubMedID 36242511
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Identification of Resolvin D1 and Protectin D1 as Potential Therapeutic Agents for Treating Kidney Stones.
Oxidative medicine and cellular longevity
2022; 2022: 4345037
Abstract
Intrarenal calcium oxalate (CaOx) crystals induce renal tubular epithelial cell (TEC) inflammatory and oxidative injury. This study is aimed at exploring potential therapeutic lipid components in kidney stones because lipids are involved in the development of several diseases and indicate the risk of kidney stones. Serum specimens were collected from 35 kidney stone patients and 35 normal controls. The lipid components in serum were measured, and differences were analyzed. The documented biological importance was comprehensively reviewed to identify lipids that differed significantly between the two groups to find potential agents associated with kidney stones. CaOx nephrocalcinosis mouse model was established to examine the therapeutic effects of specific lipids on CaOx deposition and CaOx-induced oxidative renal injury. Several lipids with significantly different levels were present in the serum of patients with stones and normal controls. Resolvin D1 (RvD1) (4.93-fold change, P < 0.001) and protectin D1 (PD1) (5.06-fold change, P < 0.001) were significantly decreased in the serum of patients with kidney stones, and an integrative review suggested that these factors might be associated with inflammatory responses, which is a crucial mechanism associated with stone damage. The administration of RvD1 and PD1 significantly inhibited kidney CaOx deposition and suppressed CaOx-induced renal tubular cell inflammatory injury and necrosis in a CaOx nephrocalcinosis mouse model. Furthermore, RvD1 and PD1 facilitated the expression of the oxidative indicator superoxide dismutase 2 (SOD2), inhibited NADPH oxidase 2 (NOX2) expression, and diminished intracellular reactive oxygen species (ROS) levels. This study preliminarily elucidated the role of lipids in kidney stones. The inhibitory effects of RvD1 and PD1 on oxidative damage induced by CaOx deposition provide a promising perspective for kidney stone treatment strategies.
View details for DOI 10.1155/2022/4345037
View details for PubMedID 35251472
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Comprehensive characteristics of pathological subtypes in testicular germ cell tumor: Gene expression, mutation and alternative splicing.
Frontiers in immunology
2022; 13: 1096494
Abstract
Background: Testicular germ cell tumor (TGCT) is the most common tumor in young men, but molecular signatures, especially the alternative splicing (AS) between its subtypes have not yet been explored.Methods: To investigate the differences between TGCT subtypes, we comprehensively analyzed the data of gene expression, alternative splicing (AS), and somatic mutation in TGCT patients from the TCGA database. The gene ontology (GO) enrichment analyses were used to explore the function of differentially expressed genes and spliced genes respectively, and Spearman correlation analysis was performed to explore the correlation between differential genes and AS events. In addition, the possible patterns in which AS regulates gene expression were elaborated by the ensemble database transcript atlas. And, we identified important transcription factors that regulate gene expression and AS and functionally validated them in TGCT cell lines.Results: We found significant differences between expression and AS in embryonal carcinoma and seminoma, while mixed cell tumors were in between. GO enrichment analyses revealed that both differentially expressed and spliced genes were enriched in transcriptional regulatory pathways, and obvious correlation between expression and AS events was determined. By analyzing the transcript map and the sites where splicing occurs, we have demonstrated that AS regulates gene expression in a variety of ways. We further identified two pivot AS-related molecules (SOX2 and HDAC9) involved in AS regulation, which were validated in embryonal carcinoma and seminoma cell lines. Differences in somatic mutations between subtypes are also of concern, with our results suggesting that mutations in some genes (B3GNT8, CAPN7, FAT4, GRK1, TACC2, and TRAM1L1) occur only in embryonal carcinoma, while mutations in KIT, KARS, and NRAS are observed only in seminoma.Conclusions: In conclusion, our analysis revealed the differences in gene expression, AS and somatic mutation among TGCT subtypes, providing a molecular basis for clinical diagnosis and precise therapy of TGCT patients.
View details for DOI 10.3389/fimmu.2022.1096494
View details for PubMedID 36713456