TRPM2: a multifunctional ion channel for calcium signalling
Open accessAbstract
The transient potential receptor melastatin‐2 (TRPM2) channel has emerged as an important Ca 2+ signalling mechanism in a variety of cells, contributing to cellular functions that include cytokine production, insulin release, cell motility and cell death. Its ability to respond to reactive oxygen species has made TRPM2 a potential therapeutic target for chronic inflammation, neurodegenerative diseases, and oxidative stress‐related pathologies. TRPM2 is a non‐selective, calcium (Ca 2+)‐permeable cation channel of the melastatin‐related transient receptor potential (TRPM) ion channel subfamily. It is activated by intracellular adenosine diphosphate ribose (ADPR) through a diphosphoribose hydrolase domain in its C‐terminus and regulated through a variety of factors, including synergistic facilitation by [Ca 2+]i, cyclic ADPR, H 2 O 2, NAADP, and negative feedback regulation by AMP and permeating protons (pH). In addition to its role mediating Ca 2+ influx into the cells, TRPM2 can also function as a lysosomal Ca 2+ release channel, contributing to cell death. The physiological and pathophysiological context of ROS‐mediated events makes TRPM2 a promising target for the development of therapeutic tools of inflammatory and degenerative diseases.
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ROS reportedly favor activation of lysosomal Ca2+ channels.
“ROS reportedly favor the activation of lysosomal Ca2+ channels [768].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [768]
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A review of TRP channels splicing
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H2O2-stimulated Ca2+ influx via TRPM2 is not the sole determinant of subsequent cell death
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Flagged first, then by citations
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- Authors
- Sumoza‐Toledo, A., & Penner, R.
- Affiliations
- University of Hawaiʻi at Mānoa (US)
- Venue
- The Journal of Physiology
- Publisher
- Wiley
- Published
- 2011-03-30
- Volume
- 589
- Issue
- 7
- Pages
- 1515-1525
- ISSN
- 0022-3751 (ISSN-L)
- 1469-7793
- PMC
- PMC3099011
- OpenAlex
- W2114610934
- Cited by
- 290
- References
- 111
- Citations by year
- 2026: 10 · 2025: 19 · 2024: 20 · 2023: 17 · 2022: 15 · 2021: 25 · 2020: 24 · 2019: 17 · 2018: 15 · 2017: 21 · 2016: 13 · 2015: 17 · 2014: 23 · 2013: 24 · 2012: 22
- FWCI
- 1.64
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Journal of Physiology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
- Life Sciences › Neuroscience › Sensory Systems › Ion Channels and Receptors
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Keywords
- TRPM2, calcium signaling, ion channels, ADP-ribosylation, reactive oxygen species, lysosomal calcium release, cell death, AMPK, NAADP, hydrogen peroxide, chronic inflammation, neurodegenerative diseases, oxidative stress, therapeutic target
- MeSH terms
- Animals, Bipolar Disorder, Diabetes Mellitus, Type 2, Humans, Models, Biological, Models, Molecular, Ion Channel Gating, Alternative Splicing, Mice, Knockout, Calcium Signaling, TRPM Cation Channels, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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