Furthermore, Myo1b gene knockdown in senescent ECs and old mice remarkably attenuates cellular senescence with concomitant restoration of endothelial function, and reduction of senescence-associated secretory phenotype (SASP) characterized by the decreased of proinflammatory cytokines releases, suggesting that Myo1b plays a crucial role in the regulation endothelial aging and aging-associated endothelial dysfunction. Here, MYO1B is linked to endothelial dysfunction.