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February 8, 2026Circulation

TRPM7 deficiency reduced infarct size and improved cardiac function after ischemia/reperfusion injury by inhibiting pyroptosis mediated by intracellular Zn2+ release.

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Why the study?

Does TRPM7 deficiency reduce infarct size and improve cardiac function in models of myocardial ischemia-reperfusion injury?

Population

Hearts from patients with ischemic heart failure, ischemia/reperfusion-injured mice, global…

Comparison

TRPM7 deficiency vs Wild-type or control models

Design

Preclinical

Key result

TRPM7 deficiency reduced infarct size and improved cardiac function after ischemia/reperfusion injury by inhibiting pyroptosis mediated by intracellular Zn2+ release.

Authors

XLXin LiXLXiaohan LiCLCindy Xintong Li

Discussion

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Member takes

Overview

Suggests TRPM7 as novel target for cardioprotection; leaves open further research into its inhibition for MI.

Key Points

  • This research explores the role of TRPM7 in myocardial ischemia-reperfusion injury and its effect on cellular zinc homeostasis.
  • Analyzed TRPM7 expression in heart tissues from ischemic heart failure patients and injured mice.
  • Employed cardiomyocyte-specific and fibroblast-specific knockout mice to assess TRPM7's role during injury.
  • Utilized primary and induced pluripotent stem cell-derived cardiomyocytes for mechanistic studies using patch-clamp and imaging techniques.
  • Created an inducible channel-dead TRPM7 mouse model to examine functional aspects.
  • TRPM7 was upregulated in hearts of ischemic patients and injured mice.
  • TRPM7 deficiency decreased infarct size and improved cardiac function after injury.
  • Protection against injury was observed primarily in cardiomyocytes, not in fibroblasts.
  • Zn release from TRPM7 vesicles during reperfusion triggered cardiomyocyte death via pyroptosis.
  • Channel function of TRPM7, rather than its kinase activity, was essential for mediating injury effects.

Structured PICO

Does TRPM7 deficiency reduce infarct size and improve cardiac function in models of myocardial ischemia-reperfusion injury?

P
Population
Hearts from patients with ischemic heart failure, ischemia/reperfusion (I/R)-injured mice, global, cardiomyocyte-specific (cmTrpm7-/-), and fibroblast-specific (fibTrpm7-/-) Trpm7 knockout mice, primary neonatal mouse cardiomyocytes, human induced pluripotent stem cell-derived cardiomyocytes, and inducible TRPM7 channel dead (TRPM7-E1047K) knock-in mice
I
Intervention
TRPM7 deficiency (via global knockout, cardiomyocyte-specific knockout, fibroblast-specific knockout, or inducible channel-dead knock-in)
C
Comparator
Wild-type or control models
O
Outcome
Infarct size and cardiac function after ischemia/reperfusion injurysurrogate

TRPM7 deficiency in cardiomyocytes protects against ischemia-reperfusion injury by preventing intracellular Zn2+ release and subsequent pyroptosis, identifying TRPM7 as a potential therapeutic target for ischemic heart disease.

Cite This Study

Li et al. (2026) studied Myocardial ischemia-reperfusion injury. TRPM7 deficiency vs. Wild-type controls was evaluated on Infarct size and cardiac function. TRPM7 deficiency reduced infarct size and improved cardiac function after ischemia/reperfusion injury by inhibiting pyroptosis mediated by intracellular Zn2+ release.

synapsesocial.com/papers/698828b90fc35cd7a88487ddhttps://doi.org/10.1161/circulationaha.125.074791
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