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Calcium signaling in lysosome-dependent cell death
Mateus Milani1, Philippe Pihán1, Claudio Hetz2
1Biomedical 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.
Calcium signaling regulates cellular processes, including lysosome-dependent cell death (LDCD). This review highlights recent advances in understanding calcium
Area of Science:
- Cell Biology
- Molecular Signaling
- Physiology
Background:
- Calcium ions (Ca2+) are vital intracellular and extracellular signal messengers.
- Calcium signaling mediates interorganelle communication, impacting cellular processes like proliferation, metabolism, and cell death.
- Lysosomal function, including lumenal pH, is modulated by calcium and lysosomal ion channels.
Purpose of the Study:
- To review the fundamental aspects of lysosome-dependent cell death (LDCD).
- To emphasize recent advancements in the role of calcium signaling in LDCD.
- To explore how calcium dynamics influence lysosomal functions and contribute to cell death pathways.
Main Methods:
- Literature review focusing on cellular calcium signaling.
- Analysis of studies investigating lysosomal ion channels and their functions.
- Synthesis of recent research on the mechanisms of lysosome-dependent cell death.
Main Results:
- Lysosomal calcium levels and ion channel activity are critical for regulating lysosomal functions.
- Dysregulation of calcium signaling contributes to aberrant lysosome-dependent cell death.
- Calcium signaling pathways are integral to the initiation and execution of LDCD.
Conclusions:
- Lysosome-dependent cell death is a key process in tissue homeostasis, development, and disease.
- Calcium signaling plays a central role in modulating LDCD.
- Further research into calcium-mediated lysosomal pathways can reveal therapeutic targets for diseases involving LDCD.
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