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High-density lipoprotein protects cardiomyocytes from oxidative stress via the PI3K/mTOR signaling pathway

Manabu Nagao1, Ryuji Toh2, Yasuhiro Irino2

  • 1Division of Cardiovascular Medicine Kobe University Graduate School of Medicine Japan.

FEBS Open Bio
|September 15, 2017
PubMed

Insights

High-density lipoprotein (HDL) protects heart cells from damage by regulating the PI3K/mTOR pathway. This finding suggests HDL may offer a new therapeutic approach for heart failure.

Area of Science:

  • Cardiovascular Biology
  • Cellular Signaling
  • Heart Failure Pathophysiology

Background:

  • Low high-density lipoprotein (HDL) cholesterol is linked to increased heart failure risk.
  • The direct impact of HDL on failing heart muscle (myocardium) remains unclear.

Purpose of the Study:

  • To investigate the direct effects of HDL on cardiomyocytes under stress.
  • To elucidate the molecular pathways mediating HDL's cardioprotective actions.

Main Methods:

  • Utilized H9c2 cardiomyocytes exposed to oxidative stress.
  • Administered HDL treatment and analyzed cell viability.
  • Investigated the role of the phosphatidylinositol 3-kinase (PI3K)/mammalian target of rapamycin (mTOR) signaling pathway.

Main Results:

  • HDL treatment significantly improved H9c2 cardiomyocyte viability under oxidative stress.
  • The cardioprotective effect of HDL was mediated by the PI3K/mTOR pathway.
  • mTOR signaling promotes cell survival by inactivating the BCL2-associated agonist of cell death.

Conclusions:

  • HDL exerts direct cardioprotective effects on cardiomyocytes.
  • Modulation of cardiac PI3K/mTOR signaling by HDL is a key mechanism.
  • HDL-mediated PI3K/mTOR pathway activation presents a potential therapeutic strategy for heart failure.

Keywords:
high‐density lipoproteinmTOR signalingoxidative stress

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