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愈合与损伤:细胞衰老的分子机制、功能及病理学

Healing and hurting: molecular mechanisms, functions, and pathologies of cellular senescence.

作者信息

Adams Peter D

机构信息

Cancer Research UK Beatson Labs, University of Glasgow, Glasgow G61 1BD, UK.

出版信息

Mol Cell. 2009 Oct 9;36(1):2-14. doi: 10.1016/j.molcel.2009.09.021.

Abstract

Cellular senescence is a proliferation arrest that is typically irreversible and caused by various cellular stresses, including excess rounds of cell division and cancer-causing genetic alterations. Senescence actively contributes to a tissue-level response to tissue wounding and incipient cancer, healing the tissue and suppressing tumor formation. However, in the long term, the same senescence program may hurt the tissue, thereby contributing to tissue aging. Tumor suppression, wound healing, and aging are each associated with inflammation, and here it is proposed that cellular senescence contributes to a "nonimmune cell" component of the tissue inflammatory response.

摘要

细胞衰老指的是一种增殖停滞,通常是不可逆的,由各种细胞应激引起,包括过多轮次的细胞分裂和致癌基因改变。衰老积极参与组织对组织损伤和早期癌症的反应,修复组织并抑制肿瘤形成。然而,从长远来看,同样的衰老程序可能会损害组织,从而导致组织老化。肿瘤抑制、伤口愈合和衰老都与炎症相关,本文提出细胞衰老促成了组织炎症反应中的“非免疫细胞”成分。

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