Evidence map›Paper›PMID 42191897›Full record

ReviewActa pharmacologica Sinica2026

TRPM7 kinase: a target for multimodal drug development in neurological disorders.

Xin-Yang Zhang, Hio Lam Ho, Zhong-Ping Feng, Hong-Shuo Sun

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In one paragraph

Review in Acta pharmacologica Sinica, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Xin-Yang Zhang *Department of Surgery, Temerty Faculty of Medicine, University of Toronto, Toronto, ON, Canada.
Hio Lam Ho *Department of Surgery, Temerty Faculty of Medicine, University of Toronto, Toronto, ON, Canada.
Zhong-Ping FengDepartment of Physiology, Temerty Faculty of Medicine, University of Toronto, Toronto, ON, Canada. zp.feng@utoronto.ca.
Hong-Shuo SunDepartment of Surgery, Temerty Faculty of Medicine, University of Toronto, Toronto, ON, Canada. hss.sun@utoronto.ca.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurological disorders impose a rising global burden and often remain challenging to treat with conventional interventions, as their pathologies arise from interconnected cascades involving ionic imbalance, oxidative stress, mitochondrial dysfunction, and neuroinflammation. Transient receptor potential melastatin 7 (TRPM7) is a bifunctional "chanzyme" combining a divalent-permeable cation channel with a C-terminal α-kinase domain. This review synthesizes current knowledge of TRPM7 kinase, including its structural organization and regulation, and surveys its physiological roles in the nervous system. Converging genetic and pharmacological evidence links TRPM7 kinase activity to diverse brain pathologies, including ischemic and hypoxic-ischemic injury, epilepsy, Alzheimer's disease, and glioblastoma. Notably, TRPM7 kinase inactivation or inhibition exerts multimodal neuroprotection by attenuating apoptosis, oxidative stress, inflammation, and cytoskeletal remodeling. We also summarize emerging small-molecule modulators that probe kinase function, while acknowledging key limitations in selectivity, potential off-target effects, and uncertain brain penetration. Beyond these pharmacological challenges, critical gaps remain in defining kinase-channel coupling, cell type-specific substrate networks, and therapeutic windows in translational models. Overall, by integrating oxidative, inflammatory, and metabolic signaling with cytoskeletal control, TRPM7 kinase represents an underexplored but promising therapeutic node for modulating the complex injury pathways that underlie many neurological disorders. TRPM7 structure and its kinase-regulated signaling pathways in neurological disease. Schematic overview of TRPM7 structure and its involvement in cytoskeletal remodeling and glioblastoma progression, glial stem cells maintenance, nuclear translocation under OGD/R, Aβ degradation in Alzheimer's disease, seizure susceptibility and ischemic-related apoptosis and neuroinflammation. Abbreviations: Aβ amyloid-beta, OGD/R oxygen-glucose deprivation/reoxygenation. Created in https://BioRender.com .

Indexed as

drug developmention channelneurological disordersTRPM7 kinase

Identifiers

PMID42191897

What Socratic holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.