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AlZaim, I.* ; Hassan, M.N.* ; Schröter, M.* ; Mannino, L.* ; Dragicevic, K.* ; Sjogaard, M.B.* ; Festa, J.* ; Dokshokova, L.* ; Weinbrenner, S. ; Tardajos Ayllon, B.* ; Hansen, B.* ; Rasmussen, R.K.* ; Christensen, J.N.* ; Wagman, O.* ; Schipper, R.* ; Cai, M.* ; Dheedene, W.* ; Bohn, A.B.* ; Farup, J.* ; Lin, L.* ; Soraggi, S.* ; Thorsen, A.D.* ; Bæk, A.* ; Thomsen, H.H.* ; von Heesen, M.* ; Conradi, L.C.* ; Evans, P.* ; Hagberg, C.E.* ; Heeren, J.* ; Emont, M.* ; Rosen, E.D.* ; Luttun, A.* ; Etzerodt, A.* ; Massier, L. ; Rydén, M.* ; Mejhert, N.* ; Blüher, M. ; Khodosevich, K.* ; Fenton, R.A.* ; Sheikh, B.N. ; Jessen, N.* ; de Rooij, L.P.M.H.* ; Kalucka, J.*

Defining the vascular niche of human adipose tissue across metabolic states.

Nat. Metab. 8, 722–740 (2026)

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Adipose tissue homeostasis depends on an intact vascular network that ensures adequate nutrient delivery and immune regulation. In obesity, vascular dysfunction, particularly within endothelial cells (ECs), contributes to inflammation and metabolic disease progression, yet the cellular organization of the human adipose vasculature remains poorly defined. Here we show, using single-cell RNA sequencing of nearly 70,000 vascular cells from human subcutaneous adipose tissue of 65 individuals, that the adipose vasculature is highly heterogeneous and consists of seven canonical EC subtypes. In addition, we identify a distinct population of ECs that display mixed endothelial, mesenchymal, adipocytic and immune transcriptional features. Computational analyses and whole-mount imaging support their presence and suggest that they emerge through endothelial-to-mesenchymal transition. Comparative analyses further reveal inflammatory and fibrotic vascular signatures in obesity and type 2 diabetes. Together, this atlas delineates the cellular complexity of the human adipose vasculature and highlights its contribution to metabolic disease.

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Publication type Article: Journal article

Document type Scientific Article

Keywords Mesenchymal Transition; Endothelial-cells; Binding; White

ISSN (print) / ISBN 2522-5812

e-ISSN 2522-5812

Journal Nature metabolism

Quellenangaben Volume: 8, Pages: 722–740

Publisher Nature Publishing Group

Publishing Place London

Reviewing status Peer reviewed

Institute(s) Helmholtz Institute for Metabolism, Obesity and Vascular Research (HI-MAG)

Grants Formas
Karolinska Institutet (Karolinska Institute)
U.S. Department of Health and Human Services (U.S. Department of Health & Human Services)
Lundbeckfonden (Lundbeck Foundation)
Deutsche Forschungsgemeinschaft (German Research Foundation)
Riisfort Fonden (Riisfort Foundation)
Vetenskapsrdet (Swedish Research Council)
Matthias Blher received personal honoraria from Amgen, AstraZeneca, Bayer, BoehringerIngelheim, Daiichi-Sankyo, Lilly, Novo Nordisk, Novartis, and Sanofi
KU Leuven (Katholieke Universiteit Leuven)
Fonds voor Watenschappelijk Onderzoek Address: HOEK 38 Leuvenseweg 38, 1000 Brussel +32-2-512 91 10
Carlsbergfondet (Carlsberg Foundation)
Novo Nordisk Fonden (Novo Nordisk Foundation)