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Kcnh2 mediates FAK/AKT-FOXO3A pathway to attenuate sepsis-induced cardiac dysfunction

Zhigang Li1,2,3,4, Yilei Meng1,2,3,4, Chang Liu1,2,3

  • 1Key Laboratory of Arrhythmias, Ministry of Education, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.

Cell Proliferation
|December 2, 2020
PubMed
Abstract

Insights

Kcnh2 channel protects against sepsis-induced cardiac dysfunction by regulating FAK/AKT-FOXO3A signaling to block cardiomyocyte apoptosis. This highlights potassium channels

Area of Science:

  • Cardiology
  • Molecular Biology
  • Sepsis Research

Background:

  • Sepsis frequently causes myocardial dysfunction, leading to high mortality.
  • The role of Kcnh2 in sepsis-associated cardiac pathology is not fully understood.

Purpose of the Study:

  • To investigate the role of Kcnh2 in sepsis-induced cardiac dysfunction (SCID).
  • To elucidate the signaling pathways involved in Kcnh2's function during sepsis.

Main Methods:

  • Septic cardiac dysfunction was induced using cecal ligation and puncture (CLP) or lipopolysaccharide (LPS) in rats.
  • Kcnh2 expression was analyzed via Western blotting.
  • Cardiac function and survival were assessed in Kcnh2 knockout and NS1643-treated rats.

Main Results:

  • Sepsis downregulated cardiac Kcnh2 expression.
  • Kcnh2 deficiency aggravated septic cardiac dysfunction, tissue damage, and apoptosis.
  • Activation of Kcnh2 with NS1643 ameliorated these effects.
  • Kcnh2 deficiency inhibited FAK/AKT signaling, leading to FOXO3A activation and cardiomyocyte apoptosis.

Conclusions:

  • Kcnh2 plays a protective role in SCID.
  • Kcnh2 regulates the FAK/AKT-FOXO3A pathway to prevent sepsis-induced myocardial apoptosis.
  • Potassium channels like Kcnh2 represent potential therapeutic targets for SCID.
Keywords:
AKTFOXO3AKcnh2apoptosissepsis-induced cardiac dysfunction

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