ArticleNature communications2025
Obesity drives depot-specific vascular remodeling in male white adipose tissue.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed.
- Angiogenic behavior of human umbilical vein endothelial cells in hydrogel containing lyophilized powder of decellularized adipose tissue from high-fat diet-fed or exercise-trained rats.Metabolism open · 2026Article
- From brown to white: Brown adipose tissue endothelial cells whiten in culture conditions.Molecular metabolism · 2026Article
- OBESITY-INDUCED ENDOTHELIAL FENESTRATION AND CAPILLARY LEAKAGE CONTRIBUTE TO INCREASED PAIN SENSATION.bioRxiv : the preprint server for biology · 2026Article
- Defining the vascular niche of human adipose tissue across metabolic states.Nature metabolism · 2026Article
- The Intimate Relationship between Adipose Tissue, Fertility, and Bone.Journal of frailty, sarcopenia and falls · 2026Review
- Non-Coding RNAs in Obesity-Driven Vascular Dysfunction: Mechanisms, EndMT, and Translational Opportunities.Chonnam medical journal · 2026Review
- Sex differences in endothelial cell biology: cellular phenotypes and molecular regulators.Frontiers in physiology · 2026Review
- Nanomedicines Against Mitochondrial Dysfunction-Induced Metabolic Diseases.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Defining the vascular niche of human adipose tissue across metabolic states.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
Obesity-driven pathological expansion of white adipose tissue (WAT) is a key driver of endothelial dysfunction. However, early vascular alterations associated with over-nutrition also serve to exacerbate WAT dysfunction. Here, we conduct a single-cell transcriptomic analysis of WAT endothelium to delineate endothelial heterogeneity and elucidate vascular alterations and its consequence in a male murine model of obesity. We demarcate depot-specific differences in subcutaneous (sWAT) and visceral WAT (vWAT) endothelium through in sillico analysis and further corroboration of our findings. Moreover, we identify a sWAT-specific fenestrated endothelial cell (EC) subtype, which declines in obese conditions. Utilizing systemic anti-VEGFA blockade and genetic Vegfa manipulation, we demonstrate that VEGFA is necessary for maintaining fenestration in sWAT. Additionally, we detect this fenestrated EC subtype in male human WAT, which undergoes reduction in individuals with obesity. Collectively, this atlas serves as a valuable tool for future studies to decipher the functional significance of different WAT EC subtypes.
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Registered trials
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 OpenQuestion graph.