衰老诱发动脉粥样硬化:衰老疗法的功效

Udani Sari Ratih, F. C. Iswanti
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引用次数: 0

摘要

衰老是一个不可避免的过程,涉及细胞层面的生理变化。内在和外在应激源的存在会造成细胞损伤,导致衰老和过早衰老。衰老细胞会激活 p53/p21 和 p16INK4a 通路,诱导细胞周期停滞,增加衰老相关β-半乳糖苷酶(SA-β-Gal)的表达,分泌 SASP(衰老相关分泌表型),导致 "炎症老化 "或与衰老相关的慢性炎症。这些早衰和 "炎性衰老 "加速了与年龄有关的疾病的发生,动脉粥样硬化就是其中之一。早衰、衰老和动脉粥样硬化之间的关系一直是发病机制、预防和治疗研究的重点。最近的研究强调了衰老剂(能够消除衰老细胞的化合物或制剂)在抑制动脉粥样硬化的发展和延缓过早衰老方面的关键作用。如果能更全面地了解衰老素在早衰和动脉粥样硬化中的作用过程和效果,就能开发出更有效的药物,减轻治疗心血管疾病的副作用,延长寿命。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Senescence-Induced Atherosclerosis: The Potency of Senolytic Therapy
The aging process is an inevitable occurrence that involves physiological changes at the cellular level. The presence of intrinsic and extrinsic stressors can cause cellular damage, leading to senescence and premature aging. Senescent cells undergo activation of the p53/p21 and p16INK4a pathways, induce cell cycle arrest, increased expression of senescence-associated beta-galactosidase (SA-β-Gal), and secretion of SASP (senescence-associated secretory phenotype), leading to "inflamm-aging" or chronic inflammation associated with senescence. These premature aging and “inflamm-aging” accelerates the occurrence of age-related diseases, one of which is atherosclerosis. The relationship between premature aging, senescence, and atherosclerosis has been a focus of research on pathogenesis, prevention, and therapy. Recent research has emphasized the crucial role of senolytics, compounds or agents capable of eliminating senescent cells, in inhibiting the progression of atherosclerosis and slowing down premature aging. Obtaining a more comprehensive understanding of the processes and effectiveness of senolytics in premature aging and atherosclerosis should facilitate the development of more potent medicines to mitigate side effects in the management of cardiovascular disease and extend longevity.
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