Ischemic heart disease (IHD) is defined as a syndrome of ischemic cardiomyopathy. Myogenesis and angiogenesis in the ischemic myocardium are important for cardiomyocyte (CM) survival, improving cardiac function and decreasing the progression of heart failure after IHD. Cellular senescence is a state of permanent irreversible cell cycle arrest caused by stress that results in a decline in cellular functions, such as proliferation, migration, homing, and differentiation. In addition, senescent cells produce the senescence-associated secretory phenotype (SASP), which affects the tissue microenvironment and surrounding cells by secreting proinflammatory cytokines, chemokines, growth factors, and extracellular matrix degradation proteins. The accumulation of cardiovascular-related senescent cells, including vascular endothelial cells (VECs), vascular smooth muscle cells (VSMCs), CMs and progenitor cells, is an important risk factor of cardiovascular diseases, such as vascular aging, atherosclerotic plaque formation, myocardial infarction (MI) and ventricular remodeling. This review summarizes the processes of angiogenesis, myogenesis and cellular senescence after IHD. In addition, this review focuses on the relationship between cellular senescence and cardiovascular disease and the mechanism of cellular senescence. Finally, we discuss a potential therapeutic strategy for MI targeting senescent cells.

Cellular repressor of E1A-stimulated genes (CREG), a novel cellular protein, was discovered in 1998. Accumulating evidence, mainly from our laboratory, has suggested that CREG plays critical roles in reducing neointimal hyperplasia, maintaining vascular homeostasis, and promoting endothelial restoration. The study of CREG has the potential to offer new insights into both prevention and treatment of proliferative vascular disease, and will help us understand the processes of vascular repair after injury. It will also contribute to the development of new therapeutic strategies and devices, such as anti-in-stent restenosis stents. The present review summarizes our research on the molecular identity of CREG, and reviews the biological activities of CREG in regulating cell differentiation, proliferation, migration, and apoptosis of vascular smooth muscle cells and endothelial cells.