HSP90 mediates the connection of multiple programmed cell death in diseases

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Abstract

Heat shock protein (HSP) 90, an important component of the molecular chaperone network, is closely concerned with cellular signaling pathways and stress response by participating in the process of maturation and activation of client proteins, playing a crucial role both in the normal and abnormal operation of the organism. In functionally defective tissues, programmed cell death (PCD) is one of the regulable fundamental mechanisms mediated by HSP90, including apoptosis, autophagy, necroptosis, ferroptosis, and others. Here, we show the complex relationship between HSP90 and different types of PCD in various diseases, and discuss the possibility of HSP90 as the common regulatory nodal in multiple PCD, which would provide a new perspective for the therapeutic approaches in disease.

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Ferroptosis: an iron-dependent form of nonapoptotic cell death.

Scott J. Dixon, Kathryn Lemberg, Michael Lamprecht … (2012)

Nonapoptotic forms of cell death may facilitate the selective elimination of some tumor cells or be activated in specific pathological states. The oncogenic RAS-selective lethal small molecule erastin triggers a unique iron-dependent form of nonapoptotic cell death that we term ferroptosis. Ferroptosis is dependent upon intracellular iron, but not other metals, and is morphologically, biochemically, and genetically distinct from apoptosis, necrosis, and autophagy. We identify the small molecule ferrostatin-1 as a potent inhibitor of ferroptosis in cancer cells and glutamate-induced cell death in organotypic rat brain slices, suggesting similarities between these two processes. Indeed, erastin, like glutamate, inhibits cystine uptake by the cystine/glutamate antiporter (system x(c)(-)), creating a void in the antioxidant defenses of the cell and ultimately leading to iron-dependent, oxidative death. Thus, activation of ferroptosis results in the nonapoptotic destruction of certain cancer cells, whereas inhibition of this process may protect organisms from neurodegeneration. Copyright © 2012 Elsevier Inc. All rights reserved.

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Apoptosis: a review of programmed cell death.

Susan A. Elmore (2007)

The process of programmed cell death, or apoptosis, is generally characterized by distinct morphological characteristics and energy-dependent biochemical mechanisms. Apoptosis is considered a vital component of various processes including normal cell turnover, proper development and functioning of the immune system, hormone-dependent atrophy, embryonic development and chemical-induced cell death. Inappropriate apoptosis (either too little or too much) is a factor in many human conditions including neurodegenerative diseases, ischemic damage, autoimmune disorders and many types of cancer. The ability to modulate the life or death of a cell is recognized for its immense therapeutic potential. Therefore, research continues to focus on the elucidation and analysis of the cell cycle machinery and signaling pathways that control cell cycle arrest and apoptosis. To that end, the field of apoptosis research has been moving forward at an alarmingly rapid rate. Although many of the key apoptotic proteins have been identified, the molecular mechanisms of action or inaction of these proteins remain to be elucidated. The goal of this review is to provide a general overview of current knowledge on the process of apoptosis including morphology, biochemistry, the role of apoptosis in health and disease, detection methods, as well as a discussion of potential alternative forms of apoptosis.

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Autophagy: cellular and molecular mechanisms.

Danielle Glick, Sandra Barth, Kay F Macleod (2010)

Autophagy is a self-degradative process that is important for balancing sources of energy at critical times in development and in response to nutrient stress. Autophagy also plays a housekeeping role in removing misfolded or aggregated proteins, clearing damaged organelles, such as mitochondria, endoplasmic reticulum and peroxisomes, as well as eliminating intracellular pathogens. Thus, autophagy is generally thought of as a survival mechanism, although its deregulation has been linked to non-apoptotic cell death. Autophagy can be either non-selective or selective in the removal of specific organelles, ribosomes and protein aggregates, although the mechanisms regulating aspects of selective autophagy are not fully worked out. In addition to elimination of intracellular aggregates and damaged organelles, autophagy promotes cellular senescence and cell surface antigen presentation, protects against genome instability and prevents necrosis, giving it a key role in preventing diseases such as cancer, neurodegeneration, cardiomyopathy, diabetes, liver disease, autoimmune diseases and infections. This review summarizes the most up-to-date findings on how autophagy is executed and regulated at the molecular level and how its disruption can lead to disease. Copyright (c) 2010 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

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Author and article information

Contributors

Fang Liu:

ORCID: http://orcid.org/0000-0001-7451-9452

fliu0825@126.com

Journal

Journal ID (nlm-ta): Cell Death Dis

Journal ID (iso-abbrev): Cell Death Dis

Title: Cell Death & Disease

Publisher: Nature Publishing Group UK (London )

ISSN (Electronic): 2041-4889

Publication date (Electronic): 5 November 2022

Publication date PMC-release: 5 November 2022

Publication date Collection: November 2022

Volume: 13

Issue: 11

Electronic Location Identifier: 929

Affiliations

[1 ]GRID grid.488482.a, ISNI 0000 0004 1765 5169, College of Pharmacy, , Hunan University of Chinese Medicine, ; Changsha, China

[2 ]Hunan Engineering Technology Center of Standardization and Function of Chinese Herbal Decoction Piece, Changsha, China

[3 ]GRID grid.454772.7, ISNI 0000 0004 5901 2284, Key Laboratory of Modern Research of TCM, Education Department of Hunan Province, ; Changsha, 410208 China

Author information

Caiwang Peng http://orcid.org/0000-0002-1365-5810

Fengyan Zhao http://orcid.org/0000-0002-3250-1526

Hengli Li http://orcid.org/0000-0001-8418-1205

Fang Liu http://orcid.org/0000-0001-7451-9452

Article

Publisher ID: 5373

DOI: 10.1038/s41419-022-05373-9

PMC ID: 9637177

PubMed ID: 36335088

SO-VID: 3d8eabb0-40a5-47d4-91ea-54e1dd04b7cc

License:

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

History

Date received : 15 July 2022

Date revision received : 19 October 2022

Date accepted : 24 October 2022

Funding

Funded by: 2022 Hunan University of Traditional Chinese Medicine Graduate Innovation Project (2022CX91).

Funded by: 2021 Hunan University of Traditional Chinese Medicine Graduate Innovation Project (2021CX53).

Funded by: FundRef https://doi.org/10.13039/501100004735, Natural Science Foundation of Hunan Province (Hunan Provincial Natural Science Foundation);

Award ID: 2022JJ30436

Award Recipient : Fang Liu

Funded by: National Natural Science Foundation of China (81704064); Outstanding Youth Program of Scientific Research of Hunan Provincial Department of Education (20B434); Natural Science Foundation of Changsha City (kq2202259).

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ScienceOpen disciplines: Cell biology

Keywords: cell death,diseases

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ScienceOpen disciplines: Cell biology

Keywords: cell death, diseases

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HSP90 mediates the connection of multiple programmed cell death in diseases

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Genes & Diseases

Most cited references 143

Ferroptosis: an iron-dependent form of nonapoptotic cell death.

Apoptosis: a review of programmed cell death.

Autophagy: cellular and molecular mechanisms.

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Cited by 8

Most referenced authors 1,886