HSPA12B Protects Against Age-Related Endothelial Cell Senescence by Regulating STING Degradation.

ABSTRACT: Cardiovascular diseases remain the leading cause of mortality worldwide, with aging as a major risk factor. Endothelial cell (EC) dysfunction, driven by cellular senescence, is central to age-related cardiomyopathy. Despite its clinical significance, the molecular mechanisms underlying endothelial senescence remain incompletely defined. In this study, we observed that the expression of the endothelial-specific gene heat shock protein family A member 12B (HSPA12B) declines significantly with age. HSPA12B deficiency in mice accelerates age-related EC senescence and cardiac dysfunction, whereas HSPA12B overexpression mitigates EC senescence, highlighting its protective role against vascular aging. Mechanistically, HSPA12B deficiency impairs X-box binding protein 1 (XBP1) transcriptional activ

SUBMITTER: Li T 

PROVIDER: S-EPMC12686555 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature