Chao Ma

All Publications

• Engineered mucus-tethering bispecific nanobodies enhance mucosal immunity against respiratory pathogens. Nature nanotechnology Zhao, L., O'Donnell, K. L., Dubey, M., Wang, Y., Martinez, N. R., Zhang, Y., Steininger, H. M., Ma, C., Mallajosyula, V., Lee, L. L., Lachmansingh, R. N., Stavitsky, S., Takematsu, E., Hoover, M. Y., Chen, H., Guo, J., Wu, A., Ma, Y., Wang, X., Nalin, A. P., Jeong, S. D., Lu, W. J., Nguyen, P. K., Clancy, C. S., Tal, M. C., Xiao, J., Longaker, M. T., Lee, A. S., Kim, B. Y., Ambrosi, T. H., Weissman, I. L., Davis, M. M., Hasenkrug, K. J., Chien, Y. H., Jiang, W., Marzi, A., Chan, C. K. 2026

  Abstract

  Despite advances in vaccine and antiviral drug development, the prevention of respiratory viral infection and transmission remains a substantial challenge worldwide. One obvious limitation of these approaches is that they do not provide robust protection at the initial site of infection, which is the respiratory mucosa. Currently, strategies to enhance mucosal immunity against respiratory pathogens remain lacking. Here we engineered mucus-tethering bispecific nanobodies designed to provide the simultaneous neutralization of viruses by binding to their surface proteins and the entrapment of viruses within the mucus by securing them to mucin. Compared with conventional non-mucus-tethering nanobodies, these mucus-tethering bispecific nanobodies demonstrated increased retention in the respiratory tract, provided enhanced protection against influenza viral infection in mice and reduced SARS-CoV-2 transmission in hamsters. Together, our findings represent a promising strategy for enhancing mucosal defences against respiratory viruses by blocking viral entry and limiting onward transmission.

  View details for DOI 10.1038/s41565-025-02107-8

  View details for PubMedID 41565781

  View details for PubMedCentralID 8023351

• Targeting cellular senescence in progenitor cells as a strategy to enhance bone regeneration by cell therapies: a systematic review of pre-clinical investigations. Stem cell research & therapy Morita, M., Damle, E. B., Shinohara, I., Murayama, M., Susuki, Y., Gao, Q., Ma, C., Chow, S. K., Goodman, S. B. 2025; 16 (1): 669

  Abstract

  With the global population aging, optimizing bone regeneration is becoming increasingly important for enhancing the quality of life among elderly individuals. Progenitor cell-based therapies, such as mesenchymal stromal cells and induced pluripotent stem cells for bone regeneration have shown challenges due to cellular senescence and the control of the differentiation processes remain significant hurdles. In particular, elevated expression of senescence markers may play a pivotal role in limiting bone regeneration. This systematic review examines how these senescence markers influence the efficacy of progenitor cell therapies and whether targeting them could improve outcomes.We conducted a systematic literature review following the PRISMA guidelines, using the PubMed, Web of Science, Embase and Scopus with the algorithm of "bone regeneration AND senescence AND marker". Data synthesis focused on human cell sources and specifically examined senescence markers related to bone regeneration.Studies using human cells were discussed in 101 papers. Based on our inclusion and exclusion criteria, 13 papers remained for our review on senescence markers in human cells within the context of bone regeneration and senescence, with and without interventional strategies. More than half of the cell sources in current aging-related studies are derived from bone marrow. Markers of aging relevant to bone regeneration include changes in cell size and morphology, increased levels of β-galactosidase (β-Gal) and Reactive Oxygen Species (ROS), and the presence of a senescence-associated secretory phenotype (SASP). Additionally, distinct senescence markers such as p16Ink4a, p21, and p53, and mitochondrial dysfunction were associated with reduced osteogenic potential and impaired regenerative capacity.Bone marrow is the most common source of cells for studies of senescence. Cellular senescence characterized by elevated expression of specific markers was consistently shown to be negatively associated with osteogenic capacity and regenerative outcomes. The most common strategies to rejuvenate senescent cells include targeting of senescence markers and oxidative stress. Among these, modulation of p53, p21, and p16 signaling pathways has been highlighted as a potential therapeutic approach for mitigating cell senescence in bone-related conditions.

  View details for DOI 10.1186/s13287-025-04767-8

  View details for PubMedID 41316412

  View details for PubMedCentralID 11010966

• Cajanin transcriptionally disrupts the Siglec15/NFATc1 signaling cascade to attenuate osteoclast fusion and bone resorption. International immunopharmacology Ma, C., Mo, L., Wang, Z., He, W., Niu, W., Goodman, S. B., Goodnough, L. H., Liu, Y. 2025; 168 (Pt 2): 115726

  Abstract

  Osteoclast fusion is a critical step for bone resorption, and its dysregulation contributes to pathological bone loss such as postmenopausal osteoporosis. Siglec15, a membrane-bound lectin, has emerged as a key regulator of osteoclast precursor recognition and fusion. Herein, it is reported that Cajanin, a natural small-molecule compound, potently inhibits osteoclastogenesis and bone resorption both in vitro and in vivo. Cajanin treatment suppressed actin ring formation, bone resorptive activity and the expression of osteoclastic markers including Ctsk and Mmp9 in a dose-dependent manner. Transcriptomic profiling revealed that Cajanin downregulated key fusion mediators such as Siglec15, DC-STAMP, OC-STAMP and NFATc1. Gene enrichment analysis identified attenuated MAPK and NF-κB signaling, which was validated by decreased phosphorylation of ERK, JNK and p38, increased IκB-α levels and reduced nuclear translocation of p65. Moreover, Cajanin significantly suppressed NFATc1 expression and nuclear localization. In an ovariectomy-induced bone loss model, Cajanin preserved trabecular bone architecture and reduced TRAP-positive osteoclasts. Collectively, these findings demonstrate that Cajanin transcriptionally disrupts the Siglec15-NFATc1 signaling axis, thereby impairing osteoclast fusion and bone resorption, and highlight its potential as a therapeutic candidate for selectively targeting pathological osteoclast fusion in osteolytic diseases.

  View details for DOI 10.1016/j.intimp.2025.115726

  View details for PubMedID 41260165

• Can alternatives to animal testing yield useful information regarding biological mechanisms and drug discovery? Journal of orthopaedic translation Gao, Q., Chow, S. K., Shinohara, I., Murayama, M., Susuki, Y., Morita, M., Ma, C., Goodman, S. B. 2025; 55: 132-145

  Abstract

  Establish alternative strategies to standard animal experiments decrease animal utilization and simultaneously enhance the reliability of biological and disease models. This review highlights advancements in three areas: in vitro culture platforms, disease modeling, and in silico simulations. We first discuss the innovative in vitro approaches, including 2D coculture systems, 3D spheroids, organoids, and organ-on-chip models, which facilitate the creation of physiologically relevant environments. Then, we focus on cell selection and characterization in disease modeling, with a particular focus on bone fracture healing and inflammation. We further review the potential of in silico simulations, including molecular docking, machine learning (ML) approaches, and pharmacokinetics-pharmacodynamics (PK/PD) modeling, to predict drug efficacy, interactions, and biological outcomes. These alternative strategies provide the potential for obtaining accurate and consistent results, thereby enhancing biomedical research and decreasing dependence on animal models. The Translational Potential of this Article: This review examines in vitro organoids, microphysiological systems, and computational models as alternatives to animal testing. These methods enhance our understanding of biological mechanisms. They also reduce the requirement for animal models. Ultimately, they help accelerate drug discovery that can directly benefit patients.

  View details for DOI 10.1016/j.jot.2025.08.005

  View details for PubMedID 41542102

  View details for PubMedCentralID PMC12799505

• Metformin Modulates Oxidative Stress in Murine Mesenchymal Stem Cells In Vitro and Alleviates Corticosteroid-Induced Inflammation and Impairment of Bone Formation. HSS journal : the musculoskeletal journal of Hospital for Special Surgery Shinohara, I., Susuki, Y., Murayama, M., Gao, Q., Cekuc, M. S., Ergul, Y. S., Morita, M., Pius, A. K., Ma, C., Chow, S. K., Goodman, S. B. 2025: 15563316251351031

  Abstract

  Long-term use of corticosteroids is a known risk factor for various bone diseases. Corticosteroids disrupt the balance between oxidative and glycolytic energy metabolism, increase oxidative stress and reactive oxygen species (ROS) associated with prolongation of inflammation, cell apoptosis, deficits in mesenchymal stem cells (MSCs), and osteoclast differentiation. Metformin, a drug for diabetes, has antioxidant properties by inhibiting nicotinamide adenine dinucleotide phosphate oxidase, which promotes the production of ROS.We sought to evaluate the effects of corticosteroid and metformin administration on MSCs in vitro.Primary bone marrow MSCs were collected from 20 mice. We evaluated prednisolone's effects on cell proliferation, oxidative stress, osteogenic differentiation, and mineralization, followed by metformin's effect on corticosteroid-induced reduction in bone formation. Metformin (1, 10, 100 µM) was tested with prednisolone 3 ng/mL. Cytokines were assessed by Luminex.Prednisolone at 3 ng/mL significantly reduced cell proliferation, while 10 µM metformin restored it. Prednisolone increased oxidative stress and was reversed by metformin in a concentration-dependent manner, particularly at 100 µM. Osteogenic differentiation and mineralization were significantly impaired with prednisolone but improved with metformin at 10 and 100 µM. As for inflammatory cytokines, interleukin-1β (IL-1β) expression was increased by prednisolone administration and suppressed by metformin. Conversely, IL-6 and monocyte chemotactic protein-1 were suppressed by prednisolone.This in vitro study found that corticosteroid-associated decrease in osteogenic potential of murine MSCs was associated with elevated oxidative stress that can be alleviated by metformin; further studies are needed to validate these findings in vivo and with human-derived MSCs.

  View details for DOI 10.1177/15563316251351031

  View details for PubMedID 40661872

  View details for PubMedCentralID PMC12255654

• Optimization of Cytometry by Time-of-Flight Staining for Peripheral Blood and Bone Marrow Samples. Tissue engineering. Part C, Methods Susuki, Y., Shinohara, I., Murayama, M., Morita, M., Ma, C., Pius, A. K., Gao, Q., Chow, S. K., Goodman, S. B. 2025; 31 (7): 261-270

  Abstract

  Cytometry by time-of-flight (CyTOF) enables comprehensive immune profiling for translational research. However, challenges such as signal variability, nonspecific binding, and antibody incompatibility can compromise data quality. This study presents an optimized CyTOF staining protocol for human peripheral blood mononuclear cells and bone marrow aspiration concentrate samples, addressing these challenges by refining antibody conjugation with polymer X8, saponin use, and fixation protocols. Preliminary data indicate improved staining for key markers (CD14, CD16, and CD19), enhancing signal consistency and clarity. These findings advance the utility of CyTOF in orthopaedic research and immune profiling for diseases such as osteonecrosis of the femoral head.

  View details for DOI 10.1177/19373341251360986

  View details for PubMedID 40690723

• Metformin Modulates Cell Oxidative Stress to Mitigate Corticosteroid-Induced Suppression of Osteogenesis in a 3D Model. Journal of inflammation research Cekuc, M. S., Ergul, Y. S., Pius, A. K., Meagan, M., Shinohara, I., Murayama, M., Susuki, Y., Ma, C., Morita, M., Chow, S. K., Bunnell, B. A., Lin, H., Gao, Q., Goodman, S. B. 2024; 17: 10383-10396

  Abstract

  Corticosteroids provide well-established therapeutic benefits; however, they are also accompanied by adverse effects on bone. Metformin is a widely used medication for managing type 2 diabetes mellitus. Recent studies have highlighted additional therapeutic benefits of metformin, particularly concerning bone health and oxidative stress.This research investigates the effects of prednisolone on cellular metabolic functions and bone formation using a 3D in vitro model. Then, we demonstrate the potential therapeutic effects of metformin on oxidative stress and the formation of calcified matrix due to corticosteroids.Human mesenchymal stem cells (MSCs) and macrophages were cultured in a 3D GelMA scaffold and stimulated with prednisolone, with and without metformin. The adverse effects of prednisolone and metformin's therapeutic effect(s) were assessed by analyzing cell viability, osteogenesis markers, bone mineralization, and inflammatory markers. Oxidative stress was measured by evaluating reactive oxygen species (ROS) levels and ATP production.Prednisolone exhibited cytotoxic effects, reducing the viability of MSCs and macrophages. Lower osteogenesis potential was also detected in the MSC group. Metformin positively affected cell functions, including enhanced osteoblast activity and increased bone mineralization. Furthermore, metformin effectively reduced oxidative stress, as evidenced by decreased ROS levels and increased ATP production. These findings indicate that metformin protects against oxidative damage, thus supporting osteogenesis.Metformin exhibits promising therapeutic potential beyond its role in diabetes management. The capacity to alleviate oxidative stress highlights the potential of metformin in supporting bone formation in inflammatory environments.

  View details for DOI 10.2147/JIR.S498888

  View details for PubMedID 39654863

  View details for PubMedCentralID PMC11625639

• The advantages and shortcomings of stem cell therapy for enhanced bone healing. Tissue engineering. Part C, Methods Chow, S. K., Gao, Q., Pius, A., Morita, M., Ergul, Y. S., Murayama, M., Shinohara, I., Cekuc, M. S., Ma, C., Susuki, Y., Goodman, S. B. 2024

  Abstract

  This review explores the regenerative potential of key progenitor cell types and therapeutic strategies to improve healing of complex fractures and bone defects. We define, summarize, and discuss the differentiation potential of totipotent, pluripotent, and multipotent stem cells, emphasizing the advantages and shortcomings of cell therapy for bone repair and regeneration. The fundamental role of mesenchymal stem cells (MSCs) is highlighted due to their multipotency to differentiate into the key lineage cells including osteoblasts, osteocytes, and chondrocytes, which are crucial for bone formation and remodeling. Hematopoietic stem cells (HSCs) also play a significant role; immune cells such as macrophages and T cells modulate inflammation and tissue repair. Osteoclasts are multi-nucleated cells that are important to bone remodeling. Vascular progenitor cells are critical to oxygen and nutrient supply. The dynamic interplay among these lineages and their microenvironment is essential for effective bone restoration. Therapies involving cells that are more than "minimally manipulated" are controversial and include embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs). ESCs, derived from early-stage embryos, possess pluripotent capabilities and have shown promise in preclinical studies for bone healing. iPSCs, reprogrammed from somatic cells, offer personalized medicine applications and can differentiate into various tissue-specific cell lines. Minimally manipulative cell therapy approaches such as the use of concentrated bone marrow aspirate (BMAC), exosomes, and various biomaterials for local delivery are explored for their effectiveness in bone regeneration. BMAC, which contains mostly immune cells but few mesenchymal and vascular progenitors, probably improves bone healing by facilitating paracrine mediated intercellular communication. Exosome isolation harnesses the biological signals and cellular byproducts that are a primary source for cell crosstalk and activation. Safe, efficacious, and cost-effective strategies to enhance bone healing using novel cellular therapies are part of a changing paradigm to modulate the inflammatory, repair and regenerative pathways to achieve earlier more robust tissue healing and improved physical function.

  View details for DOI 10.1089/ten.TEC.2024.0252

  View details for PubMedID 39311464

• Cycloastragenol prevents bone loss via inhibiting osteoclast activity in glucocorticoid-induced osteonecrosis of the femoral head: Anin vivostudy. Journal of orthopaedic translation Wang, G., Ma, C., Mo, L., Chen, J., Yuan, J., Xu, J., He, W. 2024; 45: 178-187

  Abstract

  Background: Glucocorticoid-induced osteonecrosis of the femoral head (GIONFH) is a common bone and joint disease. There is currently a lack of effective treatment for GIONFH, and the disease progression may lead to total hip arthroplasty (THA). The exact mechanism of GIONFH pathogenesis remains unsettled, and emerging evidence indicates that the overactivation of osteoclasts plays a pivotal role in the occurrence and progression of this condition. Our previous study has shown that cycloastragenol (CAG), a triterpenoid saponin with multiple bioactivities, is a natural osteoclast inhibitor and has a protective effect on bone loss. However, its effect on GIONFH remains unclear.Methods: In this study, methylprednisolone (MPS) (20mg/kg) was administered via gluteal muscle injection to female Sprague-Dawley (SD) rats to induce GIONFH, and different doses of CAG (5 and 15mg/kg) were dispensed intraperitoneally for intervention. Micro-CT screening and angiography were applied to determine the shaping of necrotic lesions, the loss of trabecular bone, and the change in the local blood supply. The molecular mechanism was established by Real-time qPCR and Western blotting. Hematoxylin and eosin (H&E) staining was performed to identify empty lacunae in the femoral head.Results: CAG treatment shanked the necrotic lesion area, inhibited the trabecular bone loss, and improved the local blood supply in the femoral head. In addition, CAG medication lowered the ratio of Tnfsf11 (encoding RANKL) to Tnfrsf11b (encoding OPG) and the expression of osteoclast-specific genes, including Acp5 and Ctsk. Consistently, CAG treatment exhibited a dose-dependent weakening effect on the expression of osteoclastogenesis and bone resorption-related proteins, including TRAP, CTSK, and MMP9. CAG addition also alleviated the occurrence of empty lacunae in the subchondral region.Conclusion: Our discoveries demonstrate that CAG is a potential option for hip preservation therapy in GIONFH patients.Translational potential of this article: The protective effect of CAG on rats with GIONFH can be translated into clinical use.

  View details for DOI 10.1016/j.jot.2024.01.009

  View details for PubMedID 38549807

• Tanshinone I attenuates estrogen-deficiency bone loss via inhibiting RANKL-induced MAPK and NF-κB signaling pathways INTERNATIONAL IMMUNOPHARMACOLOGY Ma, C., Wang, Z., Mo, L., Wang, X., Zhou, G., Yi, C., Niu, W., Liu, Y. 2024; 127: 111322

  Abstract

  This study aims to reveal the role of Tanshinone I (TI) in inhibiting osteoclast activity and bone loss in vitro and in vivo, as well as elucidate its underlying molecular mechanism.A mouse model of estrogen deficiency was used to assess the inhibitory effect of TI on osteoclast activity and subsequent bone loss. To validate the impact of TI on osteoclast formation, TRAcP staining and pseudopodia belt staining were conducted. The expressions of osteoclast-specific genes and proteins were evaluated using RT-PCR and Western Blot analyses. Additionally, immunofluorescence staining was employed to examine the effect of TI on p65 nuclear translocation and the expression level of reactive oxygen species (ROS).TI demonstrated significant efficacy in alleviating bone mass loss and suppressing osteoclast activity and function in ovariectomized mice. This outcome was predominantly ascribed to a decrease in ROS levels, thereby impeding the NF-κB signaling pathway and the translocation of p65 to the nucleus. Additionally, TI hindered the RANKL-induced phosphorylation of the MAPK signaling pathway. Moreover, TI played a role in the reduction of osteoclast-specific genes and proteins.To summarize, this study sheds light on TI's capacity to modulate various signaling pathways triggered by RANKL, effectively impeding osteoclast formation and mitigating bone loss resulting from estrogen deficiency. Consequently, TI emerges as a promising therapeutic option for estrogen-deficiency bone loss.

  View details for DOI 10.1016/j.intimp.2023.111322

  View details for Web of Science ID 001135551000001

  View details for PubMedID 38064814

• Dihydrotanshinone I attenuates estrogen-deficiency bone loss through RANKL-stimulated NF-κB, ERK and NFATc1 signaling pathways. International immunopharmacology Ma, C., Mo, L., Wang, Z., Peng, D., Zhou, C., Niu, W., Liu, Y., Chen, Z. 2023; 123: 110572

  Abstract

  Postmenopausal osteoporosis, a chronic condition that predominantly affects postmenopausal women, presents a significant impediment to their overall well-being. The condition arises from estrogen deficiency, leading to enhanced osteoclast activity. Salvia miltiorrhiza, a well-established Chinese herbal medicine with a history of clinical use for osteoporosis treatment, contains diverse active constituents that have shown inhibitory effects on osteoclast formation and bone loss. Dihydrotanshinone I (DTI), a phenanthrenonequinone compound derived from the root of Salvia miltiorrhiza, has been identified as a potential therapeutic agent, although its mechanism of action on osteoclasts remains elusive. In this study, we aimed to elucidate the inhibitory potential of DTI on RANKL-induced osteoclastogenesis. We observed the ability of DTI to effectively impede the expression of key osteoclast-specific genes and proteins, as assessed by Real-time PCR and Western Blotting analyses. Mechanistically, DTI exerted its inhibitory effects on osteoclast formation by modulating critical signaling pathways including NF-κB, ERK, and calcium ion signaling. Notably, DTI intervention disrupted the nuclear translocation and subsequent transcriptional activity of the NFATc1, thus providing mechanistic insights into its inhibitory role in osteoclastogenesis. To further assess the therapeutic potential of DTI, we employed an ovariectomized osteoporosis animal model to examine its impact on bone loss. Encouragingly, DTI demonstrated efficacy in mitigating bone loss induced by estrogen deficiency. In conclusion, our investigation elucidates the ability of DTI to regulate multiple signaling pathways activated by RANKL, leading to the inhibition of osteoclast formation and prevention of estrogen-deficiency osteoporosis. Consequently, DTI emerges as a promising candidate for the treatment of osteoporosis.

  View details for DOI 10.1016/j.intimp.2023.110572

  View details for PubMedID 37572501

• Combination of Distinct Vascular Stem/Progenitor Cells for Neovascularization and Ischemic Rescue. Arteriosclerosis, thrombosis, and vascular biology Zhao, L., Lee, A. S., Sasagawa, K., Sokol, J., Wang, Y., Ransom, R. C., Zhao, X., Ma, C., Steininger, H. M., Koepke, L. S., Borrelli, M. R., Brewer, R. E., Lee, L. L., Huang, X., Ambrosi, T. H., Sinha, R., Hoover, M. Y., Seita, J., Weissman, I. L., Wu, J. C., Wan, D. C., Xiao, J., Longaker, M. T., Nguyen, P. K., Chan, C. K. 2023

  Abstract

  Peripheral vascular disease remains a leading cause of vascular morbidity and mortality worldwide despite advances in medical and surgical therapy. Besides traditional approaches, which can only restore blood flow to native arteries, an alternative approach is to enhance the growth of new vessels, thereby facilitating the physiological response to ischemia.The ActinCreER/R26VT2/GK3 Rainbow reporter mouse was used for unbiased in vivo survey of injury-responsive vasculogenic clonal formation. Prospective isolation and transplantation were used to determine vessel-forming capacity of different populations. Single-cell RNA-sequencing was used to characterize distinct vessel-forming populations and their interactions.Two populations of distinct vascular stem/progenitor cells (VSPCs) were identified from adipose-derived mesenchymal stromal cells: VSPC1 is CD45-Ter119-Tie2+PDGFRa-CD31+CD105highSca1low, which gives rise to stunted vessels (incomplete tubular structures) in a transplant setting, and VSPC2 which is CD45-Ter119-Tie2+PDGFRa+CD31-CD105lowSca1high and forms stunted vessels and fat. Interestingly, cotransplantation of VSPC1 and VSPC2 is required to form functional vessels that improve perfusion in the mouse hindlimb ischemia model. Similarly, VSPC1 and VSPC2 populations isolated from human adipose tissue could rescue the ischemic condition in mice.These findings suggest that autologous cotransplantation of synergistic VSPCs from nonessential adipose tissue can promote neovascularization and represents a promising treatment for ischemic disease.

  View details for DOI 10.1161/ATVBAHA.122.317943

  View details for PubMedID 37051932

• Integrated Bioinformatic Analysis of the Shared Molecular Mechanisms Between Osteoporosis and Atherosclerosis. Frontiers in endocrinology Mo, L., Ma, C., Wang, Z., Li, J., He, W., Niu, W., Chen, Z., Zhou, C., Liu, Y. 2022; 13: 950030

  Abstract

  Osteoporosis and atherosclerosis are common in the elderly population, conferring a heavy worldwide burden. Evidence links osteoporosis and atherosclerosis but the exact underlying common mechanism of its occurrence is unclear. The purpose of this study is to further explore the molecular mechanism between osteoporosis and atherosclerosis through integrated bioinformatic analysis.The microarray data of osteoporosis and atherosclerosis in the Gene Expression Omnibus (GEO) database were downloaded. The Weighted Gene Co-Expression Network Analysis (WGCNA) and differentially expressed genes (DEGs) analysis were used to identify the co-expression genes related to osteoporosis and atherosclerosis. In addition, the common gene targets of osteoporosis and atherosclerosis were analyzed and screened through three public databases (CTD, DISEASES, and GeneCards). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed by Metascape. Then, the common microRNAs (miRNAs) in osteoporosis and atherosclerosis were screened out from the Human microRNA Disease Database (HMDD) and the target genes of whom were predicted through the miRTarbase. Finally, the common miRNAs-genes network was constructed by Cytoscape software.The results of common genes analysis showed that immune and inflammatory response may be a common feature in the pathophysiology of osteoporosis and atherosclerosis. Six hub genes (namely, COL1A1, IBSP, CTSD, RAC2, MAF, and THBS1) were obtained via taking interaction of different analysis results. The miRNAs-genes network showed that has-let-7g might play an important role in the common mechanisms between osteoporosis and atherosclerosis.This study provides new sights into shared molecular mechanisms between osteoporosis and atherosclerosis. These common pathways and hub genes may offer promising clues for further experimental studies.

  View details for DOI 10.3389/fendo.2022.950030

  View details for PubMedID 35937806

  View details for PubMedCentralID PMC9353191