Cardiovascular disease (CVD) remains the leading cause of mortality globally, so further investigation is required to identify its underlying mechanisms and potential targets for its prevention. The transcription factor p53 functions as a gatekeeper, regulating a myriad of genes to maintain normal cell functions. It has received a great deal of research attention as a tumor suppressor. In the past three decades, evidence has also shown a regulatory role for p53 in the heart. Basal p53 is essential for embryonic cardiac development; it is also necessary to maintain normal heart architecture and physiological function. In pathological cardiovascular circumstances, p53 expression is elevated in both patient samples and animal models. Elevated p53 plays a regulatory role via anti-angiogenesis, pro-programmed cell death, metabolism regulation, and cell cycle arrest regulation. This largely promotes the development of CVDs, particularly cardiac remodeling in the infarcted heart, hypertrophic cardiomyopathy, dilated cardiomyopathy, and diabetic cardiomyopathy. Roles for p53 have also been found in atherosclerosis and chemotherapy-induced cardiotoxicity. However, it has different roles in cardiomyocytes and non-myocytes, even in the same model. In this review, we describe the different effects of p53 in cardiovascular physiological and pathological conditions, in addition to potential CVD therapies targeting p53.

心血管疾病（CVD）仍然是全球死亡的主要原因，因此需要进一步研究以确定其潜在机制和潜在的预防目标。转录因子 p53 起着看门人的作用，调节大量基因以维持正常的细胞功能。它作为肿瘤抑制剂受到了广泛的研究关注。在过去的三十年里，证据还表明 p53 在心脏中具有调节作用。基础 p53 对于胚胎心脏发育至关重要；维持正常的心脏结构和生理功能也是必要的。在病理性心血管情况下，p53 表达在患者样本和动物模型中均升高。p53 升高通过抗血管生成、程序性细胞死亡、代谢调节和细胞周期停滞调节发挥调节作用。这在很大程度上促进了CVD的发展，特别是梗塞心脏的心脏重塑、肥厚型心肌病、扩张型心肌病和糖尿病心肌病。p53 在动脉粥样硬化和化疗引起的心脏毒性中也发挥着作用。然而，即使在同一模型中，它在心肌细胞和非肌细胞中也具有不同的作用。在这篇综述中，我们描述了 p53 在心血管生理和病理条件下的不同作用，以及针对 p53 的潜在 CVD 疗法。