Heart failure & cardiomyopathies
TRPM7 Deficiency Protects Against Myocardial Ischemia-Reperfusion Injury by Regulating Intracellular Zn 2+ Homeostasis
Authors' conclusion
TRPM7-mediated intracellular Zn2+ release contributes to myocardial I/R injury by triggering apoptotic and pyroptotic cardiomyocyte death.
Study context
- Population
- Hearts from patients with ischemic HF and I/R-injured mice; mouse cardiomyocytes and hiPSC-CMs
- Comparison
- TRPM7 deficiency vs intact TRPM7 in myocardial I/R injury
Methodological detailsknockout mouse models, knock-in mouse models, human iPSC-derived cardiomyocytes
- Knockout mouse models
- Knock-in mouse models
- Human iPSC-derived cardiomyocytes
Main finding
As reported in the abstract
- TRPM7 significantly upregulated in myocardium of patients with ischemic HF and I/R-injured mice
- Global TRPM7 deficiency markedly reduced infarct size and improved cardiac function after I/R injury
- TRPM7 deficiency in myocytes, not fibroblasts, protects against I/R injury by inhibiting pyroptosis
- Zn2+ release from intracellular TRPM7 vesicles triggers cardiomyocyte death via gasdermin-D activation and membrane pore formation
- Membrane TRPM7 inhibition did not protect mice against I/R injury
- Channel, not kinase, function of TRPM7 mediates I/R injury
Original publication
TRPM7 Deficiency Protects Against Myocardial Ischemia-Reperfusion Injury by Regulating Intracellular Zn 2+ Homeostasis. Circulation. Published 6 February 2026. doi:10.
Summarised from the published abstract; every number is checked against it