Ajmal Ahmad, Anneliesse Braden, Sazzad Khan, Jianfeng Xiao, Mohammad Moshahid Khan
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引用次数: 0
摘要
细胞衰老是细胞周期不可逆转停滞的一个关键过程,在这一过程中,细胞仍然存活,但在不同类型的压力下永久无法增殖。越来越多的证据表明,DNA损伤会随着时间的推移而加重,并触发DNA损伤应答信号,从而导致细胞衰老。细胞衰老是炎症反应持续存在的平台,也是许多与年龄相关疾病的核心原因。DNA 修复基因缺陷或衰老可导致早衰疾病。限制 DNA 损伤或衰老的治疗方法有助于拯救长寿和神经保护的表型,从而表明 DNA 损伤和衰老之间存在机理上的相互作用。在此,我们以独特的视角探讨了 DNA 损伤应答途径与衰老之间的相互影响以及它们对老年相关疾病的贡献。我们进一步总结了衰老机制和治疗方法的最新进展,探讨了现有的挑战,并提供了衰老领域的新见解和未来方向。
Crosstalk between the DNA damage response and cellular senescence drives aging and age-related diseases.
Cellular senescence is a crucial process of irreversible cell-cycle arrest, in which cells remain alive, but permanently unable to proliferate in response to distinct types of stressors. Accumulating evidence suggests that DNA damage builds over time and triggers DNA damage response signaling, leading to cellular senescence. Cellular senescence serves as a platform for the perpetuation of inflammatory responses and is central to numerous age-related diseases. Defects in DNA repair genes or senescence can cause premature aging disease. Therapeutic approaches limiting DNA damage or senescence contribute to a rescued phenotype of longevity and neuroprotection, thus suggesting a mechanistic interaction between DNA damage and senescence. Here, we offer a unique perspective on the crosstalk between the DNA damage response pathway and senescence as well as their contribution to age-related diseases. We further summarize recent progress on the mechanisms and therapeutics of senescence, address existing challenges, and offering new insights and future directions in the senescence field.
期刊介绍:
The aim of Seminars in Immunopathology is to bring clinicians and pathologists up-to-date on developments in the field of immunopathology.For this purpose topical issues will be organized usually with the help of a guest editor.Recent developments are summarized in review articles by authors who have personally contributed to the specific topic.