Plasma membrane integrity: implications for health and disease

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Abstract

Plasma membrane integrity is essential for cellular homeostasis. In vivo, cells experience plasma membrane damage from a multitude of stressors in the extra- and intra-cellular environment. To avoid lethal consequences, cells are equipped with repair pathways to restore membrane integrity. Here, we assess plasma membrane damage and repair from a whole-body perspective. We highlight the role of tissue-specific stressors in health and disease and examine membrane repair pathways across diverse cell types. Furthermore, we outline the impact of genetic and environmental factors on plasma membrane integrity and how these contribute to disease pathogenesis in different tissues.

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Most cited references 379

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Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018

Lorenzo Galluzzi, Ilio Vitale, Stuart A. Aaronson … (2018)

Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field.

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Inactivation of the ferroptosis regulator Gpx4 triggers acute renal failure in mice.

Jose Pedro Friedmann Angeli, Manuela Schneider, Bettina Proneth … (2014)

Ferroptosis is a non-apoptotic form of cell death induced by small molecules in specific tumour types, and in engineered cells overexpressing oncogenic RAS. Yet, its relevance in non-transformed cells and tissues is unexplored and remains enigmatic. Here, we provide direct genetic evidence that the knockout of glutathione peroxidase 4 (Gpx4) causes cell death in a pathologically relevant form of ferroptosis. Using inducible Gpx4(-/-) mice, we elucidate an essential role for the glutathione/Gpx4 axis in preventing lipid-oxidation-induced acute renal failure and associated death. We furthermore systematically evaluated a library of small molecules for possible ferroptosis inhibitors, leading to the discovery of a potent spiroquinoxalinamine derivative called Liproxstatin-1, which is able to suppress ferroptosis in cells, in Gpx4(-/-) mice, and in a pre-clinical model of ischaemia/reperfusion-induced hepatic damage. In sum, we demonstrate that ferroptosis is a pervasive and dynamic form of cell death, which, when impeded, promises substantial cytoprotection.

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Lipid Peroxidation: Production, Metabolism, and Signaling Mechanisms of Malondialdehyde and 4-Hydroxy-2-Nonenal

Antonio Ayala, Mario F Muñoz, Sandro Argüelles (2014)

Lipid peroxidation can be described generally as a process under which oxidants such as free radicals attack lipids containing carbon-carbon double bond(s), especially polyunsaturated fatty acids (PUFAs). Over the last four decades, an extensive body of literature regarding lipid peroxidation has shown its important role in cell biology and human health. Since the early 1970s, the total published research articles on the topic of lipid peroxidation was 98 (1970–1974) and has been increasing at almost 135-fold, by up to 13165 in last 4 years (2010–2013). New discoveries about the involvement in cellular physiology and pathology, as well as the control of lipid peroxidation, continue to emerge every day. Given the enormity of this field, this review focuses on biochemical concepts of lipid peroxidation, production, metabolism, and signaling mechanisms of two main omega-6 fatty acids lipid peroxidation products: malondialdehyde (MDA) and, in particular, 4-hydroxy-2-nonenal (4-HNE), summarizing not only its physiological and protective function as signaling molecule stimulating gene expression and cell survival, but also its cytotoxic role inhibiting gene expression and promoting cell death. Finally, overviews of in vivo mammalian model systems used to study the lipid peroxidation process, and common pathological processes linked to MDA and 4-HNE are shown.

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Author and article information

Contributors

John H. Brumell: john.brumell@sickkids.ca

Journal

Journal ID (nlm-ta): BMC Biol

Journal ID (iso-abbrev): BMC Biol

Title: BMC Biology

Publisher: BioMed Central (London )

ISSN (Electronic): 1741-7007

Publication date (Electronic): 13 April 2021

Publication date PMC-release: 13 April 2021

Publication date Collection: 2021

Volume: 19

Electronic Location Identifier: 71

Affiliations

[1 ]GRID grid.42327.30, ISNI 0000 0004 0473 9646, Cell Biology Program, Hospital for Sick Children, ; 686 Bay Street PGCRL, Toronto, ON M5G 0A4 Canada

[2 ]GRID grid.17063.33, ISNI 0000 0001 2157 2938, Department of Molecular Genetics, , University of Toronto, ; Toronto, ON M5S 1A1 Canada

[3 ]GRID grid.14003.36, ISNI 0000 0001 2167 3675, Center for Quantitative Cell Imaging and Department of Integrative Biology, , University of Wisconsin-Madison, ; Madison, WI 53706 USA

[4 ]GRID grid.17063.33, ISNI 0000 0001 2157 2938, Institute of Medical Science, , University of Toronto, ; Toronto, ON M5S 1A1 Canada

[5 ]GRID grid.42327.30, ISNI 0000 0004 0473 9646, SickKids IBD Centre, Hospital for Sick Children, ; Toronto, ON M5G 0A4 Canada

Article

Publisher ID: 972

DOI: 10.1186/s12915-021-00972-y

PMC ID: 8042475

PubMed ID: 33849525

SO-VID: 4f1975ca-17de-4ecd-9e51-e0b8fabd711a

License:

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

History

Date received : 8 November 2020

Date accepted : 1 February 2021

Funding

Funded by: FundRef http://dx.doi.org/10.13039/501100000024, Canadian Institutes of Health Research;

Award ID: FDN#154329

Award Recipient : John H. Brumell

Funded by: FundRef http://dx.doi.org/10.13039/100000009, Foundation for the National Institutes of Health;

Award ID: GM052932

Award Recipient : William M. Bement

Custom metadata

ScienceOpen disciplines: Life sciences

Keywords: plasma membrane,membrane damage,lipid peroxidation,pore formation,membrane repair,vesicle trafficking,cell biology,tissue injury,disease

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ScienceOpen disciplines: Life sciences

Keywords: plasma membrane, membrane damage, lipid peroxidation, pore formation, membrane repair, vesicle trafficking, cell biology, tissue injury, disease

Plasma membrane integrity: implications for health and disease

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Evolutionary Cell Biology

Most cited references 379

Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018

Inactivation of the ferroptosis regulator Gpx4 triggers acute renal failure in mice.

Lipid Peroxidation: Production, Metabolism, and Signaling Mechanisms of Malondialdehyde and 4-Hydroxy-2-Nonenal

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