ArticleNature communications2026
Endothelial FUNDC1 regulates metabolic reprogramming and the obesity-diabetes transition through the SIRT3/GATA2/endothelin-1 axis.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Gut Dysbiosis Promotes Myocardial Hypertrophy via GBP2b/GBP1 in Chronic Colitis.Circulation research · 2026Article
- Transcriptomic and genetic evidence highlights EHHADH in a FUNDC1-associated mitochondrial network in diabetic nephropathy.Metabolism open · 2026Article
- Venous Nanoflap Oscillations: Biomechanical Determinants and Hydrodynamic Consequences in the Deep Cerebral Venous System.International journal of molecular sciences · 2026Review
- Mitophagy as an active regulator of cardiac metabolic reprogramming.Frontiers in cardiovascular medicine · 2026Review
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Authors and funding
10 authors.
Funding
Abstract
Endothelial cell (EC) dysfunction is a hallmark of obesity and Type 2 diabetes mellitus (T2DM), yet the mechanisms linking vascular stress to systemic metabolic diseases remain unclear. Here, we investigated the role of the mitochondrial protein FUN14 domain-containing 1 (FUNDC1) in EC under nutritional overload. Using high-fat diet (HFD)-fed EC-specific Fundc1 knockout mice, human umbilical vein ECs, primary ECs, and vascular tissues from patients with obese/T2DM, we find that endothelial FUNDC1 expression is elevated under diabetic conditions, whereas its deletion protects mice from HFD-induced obesity, insulin resistance, and metabolic disorders. Mechanistically, overnutrition triggers nuclear export of the long isoform of SIRT3 (SIRT3-L) to mitochondria via FUNDC1, disinhibiting GATA2 and enhancing endothelin-1 (ET-1) production. Loss of FUNDC1 in ECs retains SIRT3-L in the nucleus, promoting GATA2 degradation and reducing ET-1. Endothelial FUNDC1 levels correlated positively with plasma ET-1 in individuals with obesity/T2DM. These findings identify endothelial FUNDC1 as a key regulator of vasculature-metabolic organ cross talks and obesity-diabetes transition.
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