World-Class Research Center, Digital Biodesign and Personalized Healthcare, I.M. Sechenov First Moscow State Medical University (Sechenov University), 119991 Moscow, Russia; Postal Address, 8-2 Trubetskaya Street, 119991, Moscow, Russia.
Cardiovasc Hematol Agents Med Chem. 2024;22(4):413-420. doi: 10.2174/0118715257275690231129101408.
Entropy is a natural process that affects all living cells, including senescence, an irreversible physiological process that impairs cell homeostasis. Age is a significant factor in disease development, and the pathogenesis of endothelial cell aging is multifactorial. Autophagy dysfunction accelerates endothelial cell aging and cell death, while autophagy preserves endothelial cell youthfulness through intracellular homeostasis and gene expression regulation. Sirt, mTORC1, and AMPK are youthfulness genes that induce autophagy by inhibiting mTOR and upregulating FIP200/Atg13/ULK1. Aged endothelial cells have decreased levels of Lamin B1, γH2AX, Ki67, BrdU, PCNA, and SA β-Gal. Maintaining healthy young endothelial cells can prevent most cardiovascular diseases. Autophagy targeting is a potential future therapeutic strategy to modify endothelial cell age and potentially slow or reverse the aging process. This article provides state-of-the-art research on the role of autophagy in endothelial cell aging. Hypothesizing that autophagy dysregulation is associated with early endothelial cell dysfunction and further clinical sequelae, including atherosclerosis formation, leading to various cardiovascular diseases.
熵是一种影响所有活细胞的自然过程，包括衰老，这是一种不可逆的生理过程，会损害细胞内稳态。年龄是疾病发展的重要因素，内皮细胞衰老的发病机制是多因素的。自噬功能障碍会加速内皮细胞衰老和细胞死亡，而自噬通过维持细胞内稳态和基因表达调控来保持内皮细胞的年轻。Sirt、mTORC1 和 AMPK 是通过抑制 mTOR 并上调 FIP200/Atg13/ULK1 来诱导自噬的年轻基因。衰老的内皮细胞中 Lamin B1、γH2AX、Ki67、BrdU、PCNA 和 SA β-Gal 的水平降低。保持健康的年轻内皮细胞可以预防大多数心血管疾病。针对自噬的靶向治疗可能是一种未来的治疗策略，可以改变内皮细胞的年龄，并可能减缓或逆转衰老过程。本文提供了自噬在内皮细胞衰老中的作用的最新研究。假设自噬失调与早期内皮细胞功能障碍以及进一步的临床后果有关，包括动脉粥样硬化形成，导致各种心血管疾病。
