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The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
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Related Experiment Video

Updated: Oct 13, 2025

Enhancing the Engraftment of Human Induced Pluripotent Stem Cell-derived Cardiomyocytes via a Transient Inhibition of Rho Kinase Activity
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Sacubitril Ameliorates Cardiac Fibrosis Through Inhibiting TRPM7 Channel.

Tian Jia1, Xiaozhi Wang2, Yiqun Tang3

  • 1State Key Laboratory of Natural Medicines, Department of Life Sciences and Technology, China Pharmaceutical University, Nanjing, China.

Frontiers in Cell and Developmental Biology
|November 15, 2021
PubMed
Summary

Sacubitril, a component of sacubitril/valsartan, treats cardiac fibrosis by inhibiting the TRPM7 channel. This action reduces fibroblast activation and cardiomyocyte programmed cell death (PCD), improving heart function.

Keywords:
Ca2+ influxPCDTRPM7cardiac fibrosissacubitril

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Area of Science:

  • Cardiovascular Biology
  • Pharmacology
  • Cellular Physiology

Background:

  • Cardiac fibrosis, a major cause of heart failure, involves cardiomyocyte programmed cell death (PCD) and fibroblast activation.
  • Aberrant calcium (Ca2+) influx through the TRPM7 channel is implicated in these pathological processes.
  • TRPM7 is a key regulator of cardiac fibrosis.

Purpose of the Study:

  • To elucidate the mechanism by which sacubitril, a component of sacubitril/valsartan, treats cardiac fibrosis.
  • To investigate the role of TRPM7 channel in the anti-fibrotic effects of sacubitril.

Main Methods:

  • In vivo studies using isoproterenol (ISO) to induce cardiac fibrosis and dysfunction.
  • In vitro studies on fibroblasts and cardiomyocytes.
  • Assessment of TRPM7 channel activity and protein expression.
  • Evaluation of transforming growth factor-β 1 (TGF-β1) and hypoxia-induced effects.

Main Results:

  • Sacubitril/valsartan ameliorated cardiac dysfunction and reduced fibrosis in vivo.
  • LBQ657, sacubitril's metabolite, attenuated TGF-β1-induced cardiac fibrosis by blocking TRPM7 channel activity.
  • LBQ657 reduced hypoxia-induced cardiomyocyte PCD by suppressing TRPM7-regulated Ca2+ influx.

Conclusions:

  • Sacubitril exerts anti-fibrotic effects by inhibiting the TRPM7 channel in both fibroblasts and cardiomyocytes.
  • Targeting TRPM7 channel represents a potential therapeutic strategy for cardiac fibrosis and heart failure.