Interleukin-35 Ameliorates Obesity-Associated Impairment of Endothelium-Dependent Vasodilation via the STAT3-MAPK/ERK-eNOS Signaling Axis

Background

Obesity impairs endothelial nitric oxide synthase (eNOS)-nitric oxide (NO) signaling, triggering chronic inflammation, endothelial dysfunction and defective vasodilation, which drives cardiometabolic diseases. Existing metabolic therapies provide only indirect vascular protection and fail to resolve residual inflammatory-mediated cardiovascular risk. As an anti-inflammatory interleukin 12 (IL-12) family cytokine, interleukin 35 (IL-35) is suppressed in obesity and exerts vascular protective effects under inflammatory conditions, yet its function and underlying mechanisms in obesity‑related endothelial vasodilator dysfunction remain undefined.