Asprosin aggravates vascular endothelial dysfunction via disturbing mitochondrial dynamics in obesity models

Area of Science:

• Endocrinology
• Cardiovascular Biology
• Mitochondrial Biology

Background:

• Asprosin (ASP) is a fasting-induced hormone implicated in metabolic disorders.
• Obesity is associated with vascular endothelial dysfunction and increased cardiovascular risk.

Purpose of the Study:

• To investigate the role of asprosin (ASP) in obesity-induced vascular endothelial dysfunction.
• To elucidate the underlying mechanisms of ASP's action on endothelial cells.

Main Methods:

• Utilized in vitro (palmitic acid-treated rat aortic endothelial cells) and in vivo (high-fat diet mice) obesity models.
• Assessed endothelial function, nitric oxide levels, oxidative stress, and signaling pathways.
• Investigated the impact of ASP on mitochondrial dynamics, specifically mitochondrial fission.

Main Results:

• Asprosin aggravated endothelial dysfunction, reducing nitric oxide bioavailability and impairing vasodilation.
• ASP promoted mitochondrial fission, a key factor in endothelial dysfunction.
• Neutralizing ASP or knocking out its adipose production ameliorated HFD-induced endothelial dysfunction.

Conclusions:

• Asprosin exacerbates vascular endothelial dysfunction in obesity by enhancing mitochondrial fission.
• ASP may serve as an early predictive biomarker for blood vessel dysfunction.
• ASP presents a potential therapeutic target for cardiovascular complications of obesity.