Ontology highlight
ABSTRACT: Background
Excessive proliferation of vascular smooth muscle cells (VSMCs) is a consequence of type 2 diabetes (T2D) that increases the risk for atherosclerosis and restenosis after angioplasty. Here, we sought to determine whether and how mitochondrial dysfunction in T2D drives VSMC proliferation with a focus on increased reactive oxygen species and intracellular [Ca2+] that both drive cell proliferation, occur in T2D, and are regulated by the mitochondrial Ca2+ uniporter (MCU).Methods
Using a mouse model of T2D, we performed in vivo phenotyping after mechanical injury and established the mechanisms of excessive proliferation in cultured VSMCs. The T2D model was induced by high-fat diet and low-dose streptozotocin in both wild type mice and mice with
SUBMITTER: Koval OM
PROVIDER: S-EPMC12449995 | biostudies-literature | 2025 Aug
REPOSITORIES: biostudies-literature