Cell death induction and protection by activation of ubiquitously expressed anion/cation channels. Part 3: the roles and properties of TRPM2 and TRPM7

Cell volume regulation (CVR) is a prerequisite for animal cells to survive and fulfill their functions. CVR dysfunction is essentially involved in the induction of cell death. In fact, sustained normotonic cell swelling and shrinkage are associated with necrosis and apoptosis, and thus called the ne...

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Main Authors: Yasunobu Okada, Tomohiro Numata, Ravshan Z. Sabirov, Makiko Kashio, Peter G. Merzlyak, Kaori Sato-Numata
Format: Article
Language:English
Published: Frontiers Media S.A. 2023-09-01
Series:Frontiers in Cell and Developmental Biology
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fcell.2023.1246955/full
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author Yasunobu Okada
Yasunobu Okada
Yasunobu Okada
Yasunobu Okada
Yasunobu Okada
Tomohiro Numata
Ravshan Z. Sabirov
Makiko Kashio
Makiko Kashio
Peter G. Merzlyak
Kaori Sato-Numata
author_facet Yasunobu Okada
Yasunobu Okada
Yasunobu Okada
Yasunobu Okada
Yasunobu Okada
Tomohiro Numata
Ravshan Z. Sabirov
Makiko Kashio
Makiko Kashio
Peter G. Merzlyak
Kaori Sato-Numata
author_sort Yasunobu Okada
collection DOAJ
description Cell volume regulation (CVR) is a prerequisite for animal cells to survive and fulfill their functions. CVR dysfunction is essentially involved in the induction of cell death. In fact, sustained normotonic cell swelling and shrinkage are associated with necrosis and apoptosis, and thus called the necrotic volume increase (NVI) and the apoptotic volume decrease (AVD), respectively. Since a number of ubiquitously expressed ion channels are involved in the CVR processes, these volume-regulatory ion channels are also implicated in the NVI and AVD events. In Part 1 and Part 2 of this series of review articles, we described the roles of swelling-activated anion channels called VSOR or VRAC and acid-activated anion channels called ASOR or PAC in CVR and cell death processes. Here, Part 3 focuses on therein roles of Ca2+-permeable non-selective TRPM2 and TRPM7 cation channels activated by stress. First, we summarize their phenotypic properties and molecular structure. Second, we describe their roles in CVR. Since cell death induction is tightly coupled to dysfunction of CVR, third, we focus on their participation in the induction of or protection against cell death under oxidative, acidotoxic, excitotoxic, and ischemic conditions. In this regard, we pay attention to the sensitivity of TRPM2 and TRPM7 to a variety of stress as well as to their capability to physicall and functionally interact with other volume-related channels and membrane enzymes. Also, we summarize a large number of reports hitherto published in which TRPM2 and TRPM7 channels are shown to be involved in cell death associated with a variety of diseases or disorders, in some cases as double-edged swords. Lastly, we attempt to describe how TRPM2 and TRPM7 are organized in the ionic mechanisms leading to cell death induction and protection.
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spelling doaj.art-6ba675997f4f485f913a5bd87206eb442023-09-29T12:03:57ZengFrontiers Media S.A.Frontiers in Cell and Developmental Biology2296-634X2023-09-011110.3389/fcell.2023.12469551246955Cell death induction and protection by activation of ubiquitously expressed anion/cation channels. Part 3: the roles and properties of TRPM2 and TRPM7Yasunobu Okada0Yasunobu Okada1Yasunobu Okada2Yasunobu Okada3Yasunobu Okada4Tomohiro Numata5Ravshan Z. Sabirov6Makiko Kashio7Makiko Kashio8Peter G. Merzlyak9Kaori Sato-Numata10National Institute for Physiological Sciences (NIPS), Okazaki, JapanDepartment of Integrative Physiology, Graduate School of Medicine, AkitaUniversity, Akita, JapanDepartment of Physiology, School of Medicine, Aichi Medical Uniersity, Nagakute, JapanDepartment of Physiology, Kyoto Prefectural University of Medicine, Kyoto, JapanCardiovascular Research Institute, Yokohama City University, Yokohama, JapanDepartment of Integrative Physiology, Graduate School of Medicine, AkitaUniversity, Akita, JapanInstitute of Biophysics and Biochemistry, National University of Uzbekistan, Tashkent, UzbekistanNational Institute for Physiological Sciences (NIPS), Okazaki, JapanDepartment of Physiology, School of Medicine, Aichi Medical Uniersity, Nagakute, JapanInstitute of Biophysics and Biochemistry, National University of Uzbekistan, Tashkent, UzbekistanDepartment of Integrative Physiology, Graduate School of Medicine, AkitaUniversity, Akita, JapanCell volume regulation (CVR) is a prerequisite for animal cells to survive and fulfill their functions. CVR dysfunction is essentially involved in the induction of cell death. In fact, sustained normotonic cell swelling and shrinkage are associated with necrosis and apoptosis, and thus called the necrotic volume increase (NVI) and the apoptotic volume decrease (AVD), respectively. Since a number of ubiquitously expressed ion channels are involved in the CVR processes, these volume-regulatory ion channels are also implicated in the NVI and AVD events. In Part 1 and Part 2 of this series of review articles, we described the roles of swelling-activated anion channels called VSOR or VRAC and acid-activated anion channels called ASOR or PAC in CVR and cell death processes. Here, Part 3 focuses on therein roles of Ca2+-permeable non-selective TRPM2 and TRPM7 cation channels activated by stress. First, we summarize their phenotypic properties and molecular structure. Second, we describe their roles in CVR. Since cell death induction is tightly coupled to dysfunction of CVR, third, we focus on their participation in the induction of or protection against cell death under oxidative, acidotoxic, excitotoxic, and ischemic conditions. In this regard, we pay attention to the sensitivity of TRPM2 and TRPM7 to a variety of stress as well as to their capability to physicall and functionally interact with other volume-related channels and membrane enzymes. Also, we summarize a large number of reports hitherto published in which TRPM2 and TRPM7 channels are shown to be involved in cell death associated with a variety of diseases or disorders, in some cases as double-edged swords. Lastly, we attempt to describe how TRPM2 and TRPM7 are organized in the ionic mechanisms leading to cell death induction and protection.https://www.frontiersin.org/articles/10.3389/fcell.2023.1246955/fullcell volume regulationapoptosisnecrosispyroptosisoxidative cell deathacidotoxic cell death
spellingShingle Yasunobu Okada
Yasunobu Okada
Yasunobu Okada
Yasunobu Okada
Yasunobu Okada
Tomohiro Numata
Ravshan Z. Sabirov
Makiko Kashio
Makiko Kashio
Peter G. Merzlyak
Kaori Sato-Numata
Cell death induction and protection by activation of ubiquitously expressed anion/cation channels. Part 3: the roles and properties of TRPM2 and TRPM7
Frontiers in Cell and Developmental Biology
cell volume regulation
apoptosis
necrosis
pyroptosis
oxidative cell death
acidotoxic cell death
title Cell death induction and protection by activation of ubiquitously expressed anion/cation channels. Part 3: the roles and properties of TRPM2 and TRPM7
title_full Cell death induction and protection by activation of ubiquitously expressed anion/cation channels. Part 3: the roles and properties of TRPM2 and TRPM7
title_fullStr Cell death induction and protection by activation of ubiquitously expressed anion/cation channels. Part 3: the roles and properties of TRPM2 and TRPM7
title_full_unstemmed Cell death induction and protection by activation of ubiquitously expressed anion/cation channels. Part 3: the roles and properties of TRPM2 and TRPM7
title_short Cell death induction and protection by activation of ubiquitously expressed anion/cation channels. Part 3: the roles and properties of TRPM2 and TRPM7
title_sort cell death induction and protection by activation of ubiquitously expressed anion cation channels part 3 the roles and properties of trpm2 and trpm7
topic cell volume regulation
apoptosis
necrosis
pyroptosis
oxidative cell death
acidotoxic cell death
url https://www.frontiersin.org/articles/10.3389/fcell.2023.1246955/full
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