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细胞衰老的进化。

On the evolution of cellular senescence.

机构信息

Campus for Ageing and Vitality, Newcastle University Institute for Ageing, Newcastle upon Tyne, UK.

Rostock University Medical Center, Institute for Biostatistics and Informatics in Medicine and Aging Research (IBIMA), Rostock, Germany.

出版信息

Aging Cell. 2020 Dec;19(12):e13270. doi: 10.1111/acel.13270. Epub 2020 Nov 9.

Abstract

The idea that senescent cells are causally involved in aging has gained strong support from findings that the removal of such cells alleviates many age-related diseases and extends the life span of mice. While efforts proceed to make therapeutic use of such discoveries, it is important to ask what evolutionary forces might have been behind the emergence of cellular senescence, in order better to understand the biology that we might seek to alter. Cellular senescence is often regarded as an anti-cancer mechanism, since it limits the division potential of cells. However, many studies have shown that senescent cells often also have carcinogenic properties. This is difficult to reconcile with the simple idea of an anti-cancer mechanism. Furthermore, other studies have shown that cellular senescence is involved in wound healing and tissue repair. Here, we bring these findings and ideas together and discuss the possibility that these functions might be the main reason for the evolution of cellular senescence. Furthermore, we discuss the idea that senescent cells might accumulate with age because the immune system had to strike a balance between false negatives (overlooking some senescent cells) and false positives (destroying healthy body cells).

摘要

衰老细胞与衰老有关这一观点,得到了这样的发现的强有力支持:清除这些细胞可缓解许多与年龄相关的疾病并延长小鼠的寿命。虽然人们正在努力将这些发现用于治疗,但重要的是要问,是什么进化力量可能导致了细胞衰老的出现,以便更好地了解我们可能试图改变的生物学。细胞衰老通常被视为一种抗癌机制,因为它限制了细胞的分裂潜力。然而,许多研究表明,衰老细胞通常也具有致癌特性。这与简单的抗癌机制的想法很难协调一致。此外,其他研究表明,细胞衰老参与伤口愈合和组织修复。在这里,我们将这些发现和观点结合起来,并讨论了这样一种可能性,即这些功能可能是细胞衰老进化的主要原因。此外,我们还讨论了这样一种观点,即衰老细胞可能会随着年龄的增长而积累,因为免疫系统必须在假阴性(忽略一些衰老细胞)和假阳性(破坏健康的体细胞)之间取得平衡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7259/7744960/2be47546f118/ACEL-19-e13270-g001.jpg

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