自噬
背景(考古学)
疾病
神经退行性变
生物
细胞存活
癌症
程序性细胞死亡
癌细胞
癌症研究
细胞生物学
细胞
线粒体
机制(生物学)
有机体
医学
细胞凋亡
病理
遗传学
认识论
哲学
古生物学
作者
Ingo Ganzleben,Markus F. Neurath,Christoph Becker
出处
期刊:Cancers
[MDPI AG]
日期:2021-11-08
卷期号:13 (21): 5575-5575
被引量:13
标识
DOI:10.3390/cancers13215575
摘要
Autophagy is a crucial general survival tactic of mammalian cells. It describes the capability of cells to disassemble and partially recycle cellular components (e.g., mitochondria) in case they are damaged and pose a risk to cell survival or simply if their resources are urgently needed elsewhere at the time. Autophagy-associated pathomechanisms have been increasingly recognized as important disease mechanisms in non-malignant (neurodegeneration, diffuse parenchymal lung disease) and malignant conditions alike. However, the overall consequences of autophagy for the organism depend particularly on the greater context in which autophagy occurs, such as the cell type or whether the cell is proliferating. In cancer, autophagy sustains cancer cell survival under challenging, i.e., resource-depleted, conditions. However, this leads to situations in which cancer cells are completely dependent on autophagy. Accordingly, autophagy represents a promising yet complex target in cancer treatment with therapeutically induced increase and decrease of autophagic flux as important therapeutic principles.
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