Adipsin alleviates cold exposure-induced coronary microvascular dysfunction through a Gα13-dependent mechanism

Area of Science:

• Cardiovascular Biology
• Endocrinology
• Environmental Health

Background:

• Cold exposure is a known risk factor for coronary microvascular dysfunction.
• Adipsin, an adipokine, has potential cardioprotective effects.
• The role of Adipsin in cold-induced cardiovascular injury requires further investigation.

Purpose of the Study:

• To investigate Adipsin's role in cold stress-induced coronary microvascular dysfunction.
• To explore the mechanisms by which Adipsin modulates cardiovascular function under cold conditions.

Main Methods:

• Adipose tissue-specific Adipsin transgenic and wild-type mice were exposed to cold (4°C) for four weeks.
• Cardiac function, fibrosis, and microvascular integrity were assessed.
• Adipsin levels were manipulated using AAV9-shRab27a, and exosomes were analyzed for functional effects.

Main Results:

• Cold exposure impaired cardiac function and coronary microvasculature, correlating with reduced Adipsin.
• Adipsin overexpression protected against cold-induced damage, while knockdown exacerbated it.
• Adipsin-enriched exosomes restored endothelial barrier function and inhibited the RhoA/Rock1 pathway.

Conclusions:

• Adipsin protects against cold stress-induced coronary microvascular and diastolic dysfunction.
• The protective effects involve Gα13-mediated inhibition of the RhoA/Rock1 pathway.
• Adipsin demonstrates therapeutic potential for cardiovascular injury related to cold exposure.