Open AccessHigh‐density lipoprotein protects cardiomyocytes from oxidative stress via the PI 3K/ mTOR signaling pathway
Author(s) -
Nagao Manabu,
Toh Ryuji,
Irino Yasuhiro,
Nakajima Hideto,
Oshita Toshihiko,
Tsuda Shigeyasu,
Hara Tetsuya,
Shinohara Masakazu,
Ishida Tatsuro,
Hirata Kenichi
Publication year - 2017
Publication title -
febs open bio
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.718
H-Index - 31
ISSN - 2211-5463
DOI - 10.1002/2211-5463.12279
Subject(s) - pi3k/akt/mtor pathway , oxidative stress , chemistry , microbiology and biotechnology , signal transduction , high density lipoprotein , protein kinase a , cholesterol , kinase , pharmacology , medicine , biology
Low levels of plasma high‐density lipoprotein ( HDL ) cholesterol are associated with an increased risk of heart failure, regardless of the presence or absence of coronary artery disease. However, the direct effects of HDL on failing myocardium have not been fully elucidated. We found that HDL treatment resulted in improved cell viability in H9c2 cardiomyocytes under oxidative stress. This cardioprotective effect of HDL was regulated via the phosphatidylinositol 3‐kinase ( PI 3K)/mammalian target of rapamycin ( mTOR ) pathway. mTOR signaling promotes cell survival through the inactivation of the BCL 2‐associated agonist of cell death via phosphorylation of ribosomal protein S6 kinase. Modulation of cardiac PI 3K/ mTOR signaling by HDL could represent a novel therapeutic strategy for heart failure.