On the evolution of cellular senescence.
On the evolution of cellular senescence.
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关于细胞衰老的演变。
DOI:
10.1111/acel.13270
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发表时间:
2020-12
期刊:
影响因子:
7.8
通讯作者:
Kirkwood TBL
中科院分区:
文献类型:
--
作者:
Kowald A;Passos JF;Kirkwood TBL
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). Cellular senescence is often regarded as an anti‐cancer mechanism although many studies have shown that senescent cells often also have carcinogenic properties. Here, we discuss the possibility that actually wound healing, tissue repair, and development might be the main reason for the evolution of cellular senescence. We also suggest that senescent cells might accumulate with age because the immune system has to strike a balance between false negatives and false positives.
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影响因子:
64.5
作者:
Burd CE;Sorrentino JA;Clark KS;Darr DB;Krishnamurthy J;Deal AM;Bardeesy N;Castrillon DH;Beach DH;Sharpless NE
通讯作者:
Sharpless NE
影响因子:
64.8
作者:
Baker DJ;Childs BG;Durik M;Wijers ME;Sieben CJ;Zhong J;Saltness RA;Jeganathan KB;Verzosa GC;Pezeshki A;Khazaie K;Miller JD;van Deursen JM
通讯作者:
van Deursen JM
DOI:
10.1146/annurev-pathol-121808-102144
发表时间:
2010
期刊:
Annual review of pathology
影响因子:
--
作者:
Coppé JP;Desprez PY;Krtolica A;Campisi J
通讯作者:
Campisi J
DOI:
10.1073/pnas.92.20.9363
发表时间:
1995-09-26
影响因子:
11.1
作者:
DIMRI, GP;LEE, XH;CAMPISI, J
通讯作者:
CAMPISI, J
影响因子:
13.1
作者:
Burton, Dominick G. A.;Stolzing, Alexandra
通讯作者:
Stolzing, Alexandra