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本文引用的文献

1
Lysosomal quality control of cell fate: a novel therapeutic target for human diseases.溶酶体质量控制细胞命运:人类疾病的新治疗靶点。
Cell Death Dis. 2020 Sep 30;11(9):817. doi: 10.1038/s41419-020-03032-5.
2
Lysosomal dysfunction and autophagy blockade contribute to autophagy-related cancer suppressing peptide-induced cytotoxic death of cervical cancer cells through the AMPK/mTOR pathway.溶酶体功能障碍和自噬阻断通过 AMPK/mTOR 通路促进自噬相关抑癌肽诱导的宫颈癌细胞的细胞毒性死亡。
J Exp Clin Cancer Res. 2020 Sep 22;39(1):197. doi: 10.1186/s13046-020-01701-z.
3
Pompe Disease: New Developments in an Old Lysosomal Storage Disorder.庞贝病:溶酶体贮积症领域的新进展
Biomolecules. 2020 Sep 18;10(9):1339. doi: 10.3390/biom10091339.
4
Palmitic acid reduces the autophagic flux in hypothalamic neurons by impairing autophagosome-lysosome fusion and endolysosomal dynamics.棕榈酸通过损害自噬体-溶酶体融合和内溶酶体动力学来降低下丘脑神经元中的自噬通量。
Mol Cell Oncol. 2020 Jul 25;7(5):1789418. doi: 10.1080/23723556.2020.1789418. eCollection 2020.
5
Microautophagy - distinct molecular mechanisms handle cargoes of many sizes.微自噬——不同的分子机制处理不同大小的货物。
J Cell Sci. 2020 Sep 9;133(17):jcs246322. doi: 10.1242/jcs.246322.
6
CDK4/6 regulate lysosome biogenesis through TFEB/TFE3.CDK4/6 通过 TFEB/TFE3 调节溶酶体生物发生。
J Cell Biol. 2020 Aug 3;219(8). doi: 10.1083/jcb.201911036.
7
Regulation of Autophagy Progress via Lysosomal Depletion by Fluvastatin Nanoparticle Treatment in Breast Cancer Cells.氟伐他汀纳米颗粒处理通过溶酶体耗竭对乳腺癌细胞自噬进程的调控
ACS Omega. 2020 Jun 22;5(25):15476-15486. doi: 10.1021/acsomega.0c01618. eCollection 2020 Jun 30.
8
Dynamic changes of autophagic flux induced by Abeta in the brain of postmortem Alzheimer's disease patients, animal models and cell models.阿尔茨海默病患者尸检脑组织、动物模型和细胞模型中由 Abeta 诱导的自噬通量的动态变化。
Aging (Albany NY). 2020 Jun 13;12(11):10912-10930. doi: 10.18632/aging.103305.
9
New Anti-Cancer Strategy to Suppress Colorectal Cancer Growth Through Inhibition of ATG4B and Lysosome Function.通过抑制ATG4B和溶酶体功能抑制结直肠癌生长的新型抗癌策略。
Cancers (Basel). 2020 Jun 10;12(6):1523. doi: 10.3390/cancers12061523.
10
Role of autophagy in regulation of cancer cell death/apoptosis during anti-cancer therapy: focus on autophagy flux blockade.自噬在抗癌治疗期间癌细胞死亡/凋亡调控中的作用:聚焦于自噬通量阻断
Arch Pharm Res. 2020 May;43(5):475-488. doi: 10.1007/s12272-020-01239-w. Epub 2020 May 26.

溶酶体作为自噬和细胞死亡的重要调节因子。

The lysosome as an imperative regulator of autophagy and cell death.

作者信息

Mahapatra Kewal Kumar, Mishra Soumya Ranjan, Behera Bishnu Prasad, Patil Shankargouda, Gewirtz David A, Bhutia Sujit Kumar

机构信息

Department of Life Science, Cancer and Cell Death Laboratory, National Institute of Technology Rourkela, Rourkela, Odisha, 769008, India.

Division of Oral Pathology, Department of Maxillofacial Surgery and Diagnostic Sciences, College of Dentistry, Jazan University, Jazan, Saudi Arabia.

出版信息

Cell Mol Life Sci. 2021 Dec;78(23):7435-7449. doi: 10.1007/s00018-021-03988-3. Epub 2021 Oct 30.

DOI:10.1007/s00018-021-03988-3
PMID:34716768
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11071813/
Abstract

Lysosomes are single membrane-bound organelles containing acid hydrolases responsible for the degradation of cellular cargo and maintenance of cellular homeostasis. Lysosomes could originate from pre-existing endolysosomes or autolysosomes, acting as a critical juncture between autophagy and endocytosis. Stress that triggers lysosomal membrane permeabilization can be altered by ESCRT complexes; however, irreparable damage to the membrane results in the induction of a selective lysosomal degradation pathway, specifically lysophagy. Lysosomes play an indispensable role in different types of autophagy, including microautophagy, macroautophagy, and chaperone-mediated autophagy, and various cell death pathways such as lysosomal cell death, apoptotic cell death, and autophagic cell death. In this review, we discuss lysosomal reformation, maintenance, and degradation pathways following the involvement of the lysosome in autophagy and cell death, which are related to several pathophysiological conditions observed in humans.

摘要

溶酶体是由单层膜包裹的细胞器,含有酸性水解酶,负责细胞内物质的降解和细胞内稳态的维持。溶酶体可起源于预先存在的内溶酶体或自溶酶体,是自噬和内吞作用之间的关键节点。触发溶酶体膜通透性改变的应激可被内体分选转运复合体(ESCRT)改变;然而,对膜的不可修复损伤会诱导一种选择性溶酶体降解途径,即自噬性溶酶体降解。溶酶体在不同类型的自噬(包括微自噬、巨自噬和伴侣介导的自噬)以及各种细胞死亡途径(如溶酶体细胞死亡、凋亡性细胞死亡和自噬性细胞死亡)中发挥着不可或缺的作用。在本综述中,我们讨论了溶酶体参与自噬和细胞死亡后的溶酶体重塑、维持和降解途径,这些途径与在人类中观察到的几种病理生理状况相关。