Department of Pharmaceutical and Pharmacological Sciences, University of Padua, Padua, Italy; Maria Paola Belloni Center for Personalized Medicine, Padova, Italy.
Maria Paola Belloni Center for Personalized Medicine, Padova, Italy.
Adv Nutr. 2023 Sep;14(5):1111-1130. doi: 10.1016/j.advnut.2023.05.014. Epub 2023 Jun 2.
Cellular senescence has long been considered a permanent state of cell cycle arrest occurring in proliferating cells subject to different stressors, used as a cellular defense mechanism from acquiring potentially harmful genetic faults. However, recent studies highlight that senescent cells might also alter the local tissue environment and concur to chronic inflammation and cancer risk by secreting inflammatory and matrix remodeling factors, acquiring a senescence-associated secretory phenotype (SASP). Indeed, during aging and age-related diseases, senescent cells amass in mammalian tissues, likely contributing to the inevitable loss of tissue function as we age. Cellular senescence has thus become one potential target to tackle age-associated diseases as well as cancer development. One important aspect characterizing senescent cells is their telomere length. Telomeres shorten as a consequence of multiple cellular replications, gradually leading to permanent cell cycle arrest, known as replicative senescence. Interestingly, in the large majority of cancer cells, a senescence escape strategy is used and telomere length is maintained by telomerase, thus favoring cancer initiation and tumor survival. There is growing evidence showing how (poly)phenols can impact telomere maintenance through different molecular mechanisms depending on dose and cell phenotypes. Although normally, (poly)phenols maintain telomere length and support telomerase activity, in cancer cells this activity is negatively modulated, thus accelerating telomere attrition and promoting cancer cell death. Some (poly)phenols have also been shown to exert senolytic activity, thus suggesting both antiaging (directly eliminating senescent cells) and anticancer (indirectly, via SASP inhibition) potentials. In this review, we analyze selective (poly)phenol mechanisms in senescent and cancer cells to discriminate between in vitro and in vivo evidence and human applications considering (poly)phenol bioavailability, the influence of the gut microbiota, and their dose-response effects.
细胞衰老长期以来一直被认为是一种增殖细胞在受到不同应激源时发生的永久性细胞周期停滞状态,被用作一种细胞防御机制,以避免获得潜在的有害遗传缺陷。然而,最近的研究强调,衰老细胞也可能通过分泌炎症和基质重塑因子来改变局部组织环境,并共同导致慢性炎症和癌症风险,从而获得衰老相关分泌表型(SASP)。事实上,在衰老和与年龄相关的疾病中,衰老细胞在哺乳动物组织中积累,这可能导致随着年龄的增长组织功能不可避免地丧失。因此,细胞衰老已成为治疗与年龄相关的疾病和癌症发展的一个潜在目标。 衰老细胞的一个重要特征是它们的端粒长度。端粒随着多次细胞复制而缩短,逐渐导致永久性细胞周期停滞,称为复制性衰老。有趣的是,在绝大多数癌细胞中,会使用衰老逃逸策略,通过端粒酶维持端粒长度,从而有利于癌症的发生和肿瘤的存活。越来越多的证据表明,(多)酚类物质可以通过不同的分子机制影响端粒维持,具体取决于剂量和细胞表型。虽然正常情况下,(多)酚类物质可以维持端粒长度并支持端粒酶活性,但在癌细胞中,这种活性会受到负调控,从而加速端粒损耗并促进癌细胞死亡。一些(多)酚类物质也表现出衰老细胞溶解活性,因此表明其具有抗衰老(直接消除衰老细胞)和抗癌(间接通过抑制 SASP)的潜力。在这篇综述中,我们分析了衰老和癌细胞中(多)酚类物质的选择性机制,以区分体外和体内证据以及人类应用,同时考虑了(多)酚类物质的生物利用度、肠道微生物群的影响及其剂量反应效应。