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真核细胞存活机制:疾病相关性及治疗干预。

Eukaryotic cell survival mechanisms: Disease relevance and therapeutic intervention.

机构信息

Apoptosis and Cell Survival Research Laboratory, Department of Biosciences, School of Biosciences and Technology, VIT University, Vellore, Tamil Nadu-632014, India.

Apoptosis and Cell Survival Research Laboratory, Department of Biosciences, School of Biosciences and Technology, VIT University, Vellore, Tamil Nadu-632014, India.

出版信息

Life Sci. 2018 Jul 15;205:73-90. doi: 10.1016/j.lfs.2018.05.002. Epub 2018 May 4.

Abstract

Cell responds to stress by activating various modes of stress responses which aim for minimal damage to cells and speedy recovery from the insults. However, unresolved stresses exceeding the tolerance limit lead to cell death (apoptosis, autophagy etc.) that helps to get rid of damaged cells and protect cell integrity. Furthermore, aberrant stress responses are the hallmarks of several pathophysiologies (neurodegeneration, metabolic diseases, cancer etc.). The catastrophic remodulation of stress responses is observed in cancer cells in favor of their uncontrolled growth. Whereas pro-survival stress responses redirected to death signaling provokes excessive cell death in neurodegeneration. Clear understanding of such mechanistic link to disease progression is required in order to modulate these processes for new therapeutic targets. The current review explains this with respect to novel drug discoveries and other breakthroughs in therapeutics.

摘要

细胞通过激活各种应激反应模式来应对应激,这些模式旨在将细胞损伤最小化,并迅速从损伤中恢复。然而,超过耐受极限的未解决的应激会导致细胞死亡(凋亡、自噬等),这有助于清除受损细胞并保护细胞完整性。此外,异常的应激反应是几种病理生理学(神经退行性变、代谢疾病、癌症等)的特征。在有利于其不受控制生长的癌细胞中观察到应激反应的灾难性重塑。而向死亡信号重新定向的促生存应激反应会在神经退行性变中引起过度细胞死亡。为了为新的治疗靶点调节这些过程,需要清楚地了解这些与疾病进展的机制联系。本综述针对新药发现和治疗学的其他突破对此进行了解释。

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