Cell death pathology: Cross-talk with autophagy and its clinical implications

被引：68

作者：

Amelio, Ivano ^{[1
]}

Melino, Gerry ^{[1
,2
,3
]}

Knight, Richard A. ^{[1
]}

机构：

[1] Univ Leicester, Toxicol Unit, Med Res Council, Leicester LE1 9HN, Leics, England

[2] Univ Roma Tor Vergata, Biochem IDI IRCCS Lab, I-00133 Rome, Italy

[3] Univ Roma Tor Vergata, Dept Expt Med, I-00133 Rome, Italy

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2011年 / 414卷 / 02期

基金：

英国医学研究理事会;

关键词：

Autophagy; Programmed cell death; Apoptosis; Cancer; p53; P73 INDUCES APOPTOSIS; NEGATIVE REGULATION; MAMMALIAN TARGET; INHIBITION; RESISTANCE; INDUCTION; MTOR; NEURODEGENERATION; ACTIVATION; HUNTINGTIN;

D O I：

10.1016/j.bbrc.2011.09.080

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Autophagy is a self-digesting mechanism that cells adopt to respond to stressful stimuli. Morphologically, cells dying by autophagy show multiple cytoplasmic double-membraned vacuoles, and, if prolonged, autophagy can lead to cell death, "autophagic cell death". Thus, autophagy can act both as a temporary protective mechanism during a brief stressful episode and be a mode of cell death in its own right. In this mini-review we focus on recent knowledge concerning the connection between autophagy and programmed cell death, evaluating their possible implications for therapy in pathologies like cancer and neurodegeneration. (C) 2011 Elsevier Inc. All rights reserved.

引用

页码：277 / 281

页数：5

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