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Sacubitril/valsartan attenuates hypoxia/reoxygenation-induced cardiomyocyte injury by modulating macrophage

Nan Jin1, Bin Nie1, Lu Zhu1

  • 1Department of Geriatrics, The Sixth Hospital of Wuhan, Affiliated Hospital of Jianghan University, Wuhan 430015, China.

Revista De Investigacion Clinica; Organo Del Hospital De Enfermedades De La Nutricion
|April 11, 2026
PubMed

Insights

Sacubitril/valsartan (Sac/Val) protects heart cells from injury after myocardial infarction (MI) by promoting beneficial M2 macrophage polarization. This mechanism involves suppressing the TLR4/NF-κB inflammatory pathway, reducing cardiomyocyte apoptosis and inflammation.

Area of Science:

  • Cardiovascular Research
  • Immunology
  • Pharmacology

Background:

  • Cardiomyocyte apoptosis and inflammation are key drivers of myocardial infarction (MI) progression.
  • Sacubitril/valsartan (Sac/Val), an angiotensin receptor-neprilysin inhibitor, shows therapeutic promise for MI.
  • The precise cardioprotective mechanisms of Sac/Val in MI require further elucidation.

Purpose of the Study:

  • To investigate the cardioprotective effects of Sacubitril/valsartan (Sac/Val) in a myocardial infarction (MI) model.
  • To explore the role of macrophage polarization and TLR4/NF-κB signaling in Sac/Val's mechanism of action.

Main Methods:

  • Human cardiomyocytes (AC16) were pretreated with Sac/Val and subjected to hypoxia-reoxygenation (H/R) to simulate MI.
  • THP-1 macrophages were polarized, and their conditioned medium was used for co-culture with AC16 cells.
  • Cell viability, apoptosis, cytokine production, and protein expression were assessed; TLR4 signaling was inhibited using TAK242.

Main Results:

  • Sac/Val treatment improved AC16 cell viability, reduced apoptosis, and decreased pro-inflammatory cytokine release under H/R conditions.
  • Sac/Val promoted M2 macrophage polarization while inhibiting M1 polarization, concurrently suppressing TLR4/NF-κB signaling.
  • Conditioned medium from Sac/Val- or TAK242-treated macrophages attenuated H/R-induced AC16 cell injury.

Conclusions:

  • Sac/Val confers cardioprotection against hypoxia-reoxygenation injury in cardiomyocytes.
  • This protection is mediated by promoting M2 macrophage polarization and inhibiting the TLR4/NF-κB signaling pathway.
Abstract

Keywords:
CardiomyocyteHypoxia/reoxygenationMacrophage polarizationSacubitril/valsartanTLR4/NF-κB

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