Minocycline promotes cardiomyocyte mitochondrial autophagy and cardiomyocyte autophagy to prevent sepsis-induced cardiac dysfunction by Akt/mTOR signaling

Myocardial damage is responsible for the high mortality of sepsis. However, the underlying mechanism is not well understood. Cardiomyocyte autophagy alleviates the cardiac injury caused by myocardial infarction. Enhanced cardiomyocyte autophagy also has protective effects against cardiomyocyte mitoc...

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Veröffentlicht in:	Apoptosis (London) 2019-04, Vol.24 (3-4), p.369-381
Hauptverfasser:	Zhang, Erfei, Zhao, Xiaoying, Zhang, Li, Li, Nan, Yan, Jinqi, Tu, Ke, Yan, Ruhu, Hu, Jianqiang, Zhang, Mingming, Sun, Dongdong, Hou, Lichao
Format:	Artikel
Sprache:	eng
Schlagworte:	AKT protein Animals Antibiotics Autophagy Autophagy - drug effects Biochemistry Biomedical and Life Sciences Biomedicine Cancer Research Cardiac function Cardiomyocytes Cell Biology Health aspects Heart Heart attack Infection Injury prevention Kinases Male Mice Mice, Inbred C57BL Minocycline Minocycline - pharmacology Mitochondria Mitochondria - drug effects Mitochondria - metabolism Myocardial infarction Myocardial Infarction - drug therapy Myocardial Infarction - metabolism Myocardium - metabolism Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Oncology Phagocytosis Phosphorylation Phosphorylation - drug effects Proteins Proto-Oncogene Proteins c-akt - metabolism Sepsis Sepsis - drug therapy Sepsis - metabolism Signal Transduction - drug effects TOR protein TOR Serine-Threonine Kinases - metabolism Up-Regulation - drug effects Virology
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