Frataxin Loss Promotes Angiotensin II-Induced Endothelial-to-Mesenchymal Transition.

ABSTRACT:

Background

The metabolic flexibility of endothelial cells is linked to their phenotypic plasticity. Frataxin is critical in determining the iron metabolism and fate of endothelial cells. This study aimed to investigate frataxin-mediated metabolic remodeling during the endothelial-to-mesenchymal transition (EndoMT).

Methods and results

Endothelial cell-specific frataxin knockout and frataxin mutation mice were subjected to angiotensin II to induce hypertension. EndoMT and cardiac fibrosis were assessed using histological and protein expression analyses. Fatty acid oxidation (FAO) in microvascular endothelial cells was measured using a Seahorse XF96 analyzer. We showed that inhibition of FAO accompanies angiotensin II-induced EndoMT. Frataxin knockout mice promote EndoMT, asso

SUBMITTER: Guo Y 

PROVIDER: S-EPMC11964068 | biostudies-literature | 2024 Aug

REPOSITORIES: biostudies-literature