ArticleJVS-vascular science2025
Vascular adhesion molecule 1
Article in JVS-vascular science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Donor-matched iPSC model reveals context-dependent T2D genetic signals in fibro-adipogenic progenitors.bioRxiv : the preprint server for biology · 2026Article
- From fibro/adipogenic progenitors to adipocytes: Understanding adipogenesis in muscle degeneration for disease modulation.The Journal of physiology · 2025Review
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16 authors.
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Abstract
Background: Skeletal muscle health and function are critical determinants of clinical outcomes in peripheral arterial disease. Chronic limb-threatening ischemia (CLTI), the most severe clinical manifestation of peripheral arterial disease, is associated with a 1-year amputation rate of 25%. In patients with CLTI, myosteatosis-the ectopic deposition of adipocytes-is independently associated with amputation. The mechanisms responsible for myosteatosis in patients with CLTI remain unknown. In this study, we aim to identify both the causal cellular population and the molecular mechanisms in patients with CLTI that promote myosteatosis. Methods: To identify a candidate causal cell type and putative signaling axis that promotes myosteatosis, we performed single cell transcriptomic and chromatin accessibility profiling of ischemic muscle in a preclinical CLTI model. To assess the adipogenic potential for candidate subpopulations, we used an in vitro adipogenesis assay; myosteatosis was determined by Oil Red O (ORO), perilipin, and peroxisome proliferator-activated receptor gamma (PPAR-γ) staining. To determine the necessity of candidate transcriptional and epigenetic regulators, we used a small interfering RNA (siRNA). Finally, to assess the clinical significance of our findings, we used a publicly available human CLTI single cell RNA-sequencing dataset. Results: Bulk-RNA sequencings and ORO staining reveal myosteatosis as a hallmark feature of the CLTI limb. Bioinformatic analyses reveal vascular adhesion molecule 1 (Vcam1) Conclusions: Collectively, our results identify a pro-adipogenic FAP subpopulation in patients with CLTI and provide a potential therapeutic target for myosteatosis in patients with CLTI. Clinical Relevance: Myosteatosis, the pathological accumulation of fat within skeletal muscle, is increasingly recognized as a critical determinant of adverse clinical outcomes in peripheral arterial disease (PAD). Current therapies for PAD focus on revascularization and risk factor modification, but do not directly target myopathy. There is a critical need for regenerative and cellular therapies to restore muscle integrity and function. This study addresses this need by identifying a candidate causal cellular population, Vcam1
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.