While GAS5 has been demonstrated to function in a manner that exacerbates conditions like myocardial infarction [121], atherosclerosis [103], and hypoxia/reoxygenation injury [117] by promoting apoptosis, inflammation, and fibrosis, it also exhibits protective effects, such as mitigating cardiac fibrosis [112] and countering endothelial progenitor cell senescence [114]. Here, GAS5 is linked to atherosclerosis.