Qiliqiangxin Attenuates Oxidative Stress-Induced Mitochondrion-Dependent Apoptosis in Cardiomyocytes via PI3K/AKT/GSK3β Signaling Pathway

Author:

Zhao Qifei1,Li Hongrong1,Chang Liping23,Wei Cong34,Yin Yujie2,Bei Hongying2,Wang Zhixin34,Liang Junqing35,Wu Yiling12

Affiliation:

1. Department of Integrated Traditional Chinese and Western Medicine, Hebei Medical University

2. Key Disciplines of State Administration of TCM for Collateral Disease, Affiliated Yiling Hospital of Hebei Medical University

3. National Key Laboratory of Collateral Disease Research and Innovative Chinese Medicine, Hebei Yiling Pharmaceutical Research Institute

4. Key Laboratory of State Administration of TCM (Cardio-Cerebral Vessel Collateral Disease)

5. Key Laboratory of Hebei Province for Collateral Diseases

Publisher

Pharmaceutical Society of Japan

Subject

Pharmaceutical Science,Pharmacology,General Medicine

Reference41 articles.

1. 1) Leoni G, Soehnlein O. (Re)solving repair after myocardial infarction. Front Pharmacol., 9, 1342 (2018).

2. 2) Ayoub KF, Pothineni NVK, Rutland J, Ding Z, Mehta JL. Immunity, inflammation, and oxidative stress in heart failure: emerging molecular targets. Cardiovasc. Drugs Ther., 31, 593–608 (2017).

3. 3) Hou L, Guo J, Xu F, Weng X, Yue W, Ge J. Cardiomyocyte dimethylarginine dimethylaminohydrolase1 attenuates left-ventricular remodeling after acute myocardial infarction: involvement in oxidative stress and apoptosis. Basic Res. Cardiol., 113, 28 (2018).

4. 4) van der Pol A, van Gilst WH, Voors AA, van der Meer P. Treating oxidative stress in heart failure: past, present and future. Eur. J. Heart Fail., 21, 425–435 (2019).

5. 5) Torrealba N, Aranguiz P, Alonso C, Rothermel BA, Lavandero S. Mitochondria in structural and functional cardiac remodeling. Adv. Exp. Med. Biol., 982, 277–306 (2017).

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