细胞衰老（CS）是细胞周期和增殖的永久且不可逆的停滞，导致细胞结构和功能退化，与各种关键的生理和病理过程有关，特别是在癌症中。最初，CS 被认为是肿瘤发生的屏障，是保护细胞免遭恶性转化的内在防御机制。然而，越来越多的证据表明，衰老细胞可以促进肿瘤进展为明显的恶性肿瘤，主要是通过一组称为衰老相关分泌表型（SASP）的因素，包括趋化因子、生长因子、细胞因子和基质金属蛋白酶。这些因素显着重塑肿瘤微环境（TME），使肿瘤能够逃避免疫破坏。有趣的是，一些研究还表明 SASP 可能通过增强免疫监视来阻止肿瘤的发展。这些相反的作用凸显了 CS 和 SASP 在不同癌症中的复杂性和异质性。因此，人们对癌症治疗中针对 CS 或 SASP 的药物干预越来越感兴趣，例如 senolytics 和 senomorphics，以促进衰老细胞的清除或减轻 SASP 的有害影响。在这篇综述中，我们将解读CS的概念，深入探讨SASP在重塑TME中的作用，并总结针对CS或SASP的抗肿瘤策略的最新进展。© 2024。作者。

Cellular senescence (CS), a permanent and irreversible arrest of the cell cycle and proliferation leading to the degeneration of cellular structure and function, has been implicated in various key physiological and pathological processes, particularly in cancer. Initially, CS was recognized as a barrier to tumorigenesis, serving as an intrinsic defense mechanism to protect cells from malignant transformation. However, increasing evidence suggests that senescent cells can promote tumor progression to overt malignancy, primarily through a set of factors known as senescence-associated secretory phenotypes (SASPs), including chemokines, growth factors, cytokines, and stromal metalloproteinases. These factors significantly reshape the tumor microenvironment (TME), enabling tumors to evade immune destruction. Interestingly, some studies have also suggested that SASPs may impede tumor development by enhancing immunosurveillance. These opposing roles highlight the complexity and heterogeneity of CS and SASPs in diverse cancers. Consequently, there has been growing interest in pharmacological interventions targeting CS or SASPs in cancer therapy, such as senolytics and senomorphics, to either promote the clearance of senescent cells or mitigate the harmful effects of SASPs. In this review, we will interpret the concept of CS, delve into the role of SASPs in reshaping the TME, and summarize recent advances in anti-tumor strategies targeting CS or SASPs.© 2024. The Author(s).