Abstract
Abstract
Vascular senescence is a central driver of whole-body ageing, yet rescue strategies remain limited. Here we show that hydrogen sulfide (H
₂
S) bioavailability declines in ageing and atherosclerosis and is associated with endothelial senescence. Developing a novel remote-control, endothelial-specific, mitochondria-targeted chemogenetic system, we spatiotemporally controlled H
₂
S generation and thereby mitigated endothelial senescence-driven programs and reversed vascular remodeling in aged mice.