Calcium signaling in lysosome-dependent cell death.

Calcium Signaling Calcium / metabolism Cell Death Lysosomes / metabolism Intracellular Membranes / metabolism
Calcium Lysosome Lysosome membrane permeabilization Lysosome-dependent cell death

Journal

Cell calcium
ISSN: 1532-1991
Titre abrégé: Cell Calcium
Pays: Netherlands
ID NLM: 8006226

Informations de publication

Date de publication:
07 2023
Historique:
received: 02 03 2023
revised: 30 04 2023
accepted: 03 05 2023
medline: 21 6 2023
pubmed: 14 5 2023
entrez: 13 5 2023
Statut: ppublish

Résumé

Calcium is a crucial messenger of intracellular and extracellular signals, regulating a great variety of cellular processes such as cell death, proliferation, and metabolism. Inside the cell, calcium signaling is one of the main interorganelle communication mediators, with central functional roles at the endoplasmic reticulum (ER), mitochondria, Golgi complex, and lysosomes. Lysosomal function is highly dependent on lumenal calcium and most of the lysosomal membrane-localised ion channels regulate several lysosomal functions and properties such as lumenal pH. One of these functions configures a specific type of cell death involving lysosomes, named lysosome-dependent cell death (LDCD), which contributes to maintenance of tissue homeostasis, development and pathology when deregulated. Here, we cover the fundamental aspects of LDCD with a special focus on recent advances in calcium signaling in LDCD.

Identifiants

DOI: 10.1016/j.ceca.2023.102751 PMID: 37178674
pubmed: 37178674
pii: S0143-4160(23)00063-5
doi: 10.1016/j.ceca.2023.102751
pii:
doi:

Substances chimiques

Calcium SY7Q814VUP

Types de publication

Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S.

Langues

eng

Sous-ensembles de citation

IM

Pagination

102751

Informations de copyright

Copyright © 2023 Elsevier Ltd. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Mateus Milani (M)

Biomedical Neuroscience Institute (BNI), Faculty of Medicine, University of Chile, Santiago, Chile; FONDAP Center for Geroscience, Brain Health, and Metabolism (GERO), Santiago, Chile; Program of Cellular and Molecular Biology, Institute of Biomedical Sciences, University of Chile, Santiago, Chile.

Philippe Pihán (P)

Biomedical Neuroscience Institute (BNI), Faculty of Medicine, University of Chile, Santiago, Chile; FONDAP Center for Geroscience, Brain Health, and Metabolism (GERO), Santiago, Chile; Program of Cellular and Molecular Biology, Institute of Biomedical Sciences, University of Chile, Santiago, Chile.

Claudio Hetz (C)

Biomedical Neuroscience Institute (BNI), Faculty of Medicine, University of Chile, Santiago, Chile; FONDAP Center for Geroscience, Brain Health, and Metabolism (GERO), Santiago, Chile; Program of Cellular and Molecular Biology, Institute of Biomedical Sciences, University of Chile, Santiago, Chile; Buck Institute for Research on Aging, Novato, CA 94945, United States of America. Electronic address: chetz@uchile.cl.

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Classifications MeSH

questionsmedicales.fr › Phénomènes physiologiques cellulaires › Transduction du signal › Systèmes de seconds messagers › Signalisation calcique › Calcium signaling in lysosome-dependent cell death.
questionsmedicales.fr › Facteurs biologiques › Facteurs de la coagulation sanguine › Calcium › Calcium signaling in lysosome-dependent cell death.
questionsmedicales.fr › Phénomènes physiologiques cellulaires › Mort cellulaire › Calcium signaling in lysosome-dependent cell death.
questionsmedicales.fr › Cellules › Structures cellulaires › Espace intracellulaire › Cytoplasme › Structures cytoplasmiques › Organites › Vésicules cytoplasmiques › Lysosomes › Calcium signaling in lysosome-dependent cell death.
questionsmedicales.fr › Cellules › Structures cellulaires › Fractions subcellulaires › Membranes intracellulaires › Calcium signaling in lysosome-dependent cell death.