M
Mao Zhang
Researcher at Peking University
Publications - 13
Citations - 1053
Mao Zhang is an academic researcher from Peking University. The author has contributed to research in topics: Heart failure & Medicine. The author has an hindex of 7, co-authored 10 publications receiving 737 citations. Previous affiliations of Mao Zhang include Cardiovascular Institute of the South.
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Journal ArticleDOI
CaMKII is a RIP3 substrate mediating ischemia- and oxidative stress-induced myocardial necroptosis
Ting Zhang,Yan Zhang,Mingyao Cui,Li Jin,Yimei Wang,Fengxiang Lv,Yuli Liu,Wen Zheng,Haibao Shang,Jun Zhang,Mao Zhang,Hong-Kun Wu,Jiaojiao Guo,Xiuqin Zhang,Xinli Hu,Chun-Mei Cao,Rui-Ping Xiao +16 more
TL;DR: It is shown that receptor-interacting protein 3 (RIP3) triggers myocardial necroptosis, in addition to apoptosis and inflammation, through activation of Ca2+-calmodulin–dependent protein kinase (CaMKII) rather than through the well-established RIP3 partners RIP1 and MLKL.
Journal ArticleDOI
Central role of E3 ubiquitin ligase MG53 in insulin resistance and metabolic disorders
Ruisheng Song,Wei Peng,Yan Zhang,Fengxiang Lv,Hong-Kun Wu,Jiaojiao Guo,Yongxing Cao,Yanbin Pi,Xin Zhang,Li Jin,Mao Zhang,Peng Jiang,Fenghua Liu,Shaoshuai Meng,Xiuqin Zhang,Ping Jiang,Chun-Mei Cao,Rui-Ping Xiao +17 more
TL;DR: In this article, muscle-specific mitsugumin 53 (MG53; also called TRIM72) mediates the degradation of the insulin receptor and insulin receptor substrate 1 (IRS1), and when upregulated, causes metabolic syndrome featuring insulin resistance, obesity, hypertension and dyslipidaemia.
Journal ArticleDOI
Hominoid-Specific De Novo Protein-Coding Genes Originating from Long Non-Coding RNAs
Chen Xie,Yong Zhang,Jia-Yu Chen,Chu-Jun Liu,Wei-Zhen Zhou,Ying Li,Mao Zhang,Rongli Zhang,Liping Wei,Chuan-Yun Li +9 more
TL;DR: It is suggested that at least a portion of long non-coding RNAs, especially those with active and regulated transcription, may serve as a birth pool for protein-c coding genes, which are then further optimized at the transcriptional level.
Journal ArticleDOI
Programmed necrosis in cardiomyocytes: mitochondria, death receptors and beyond.
TL;DR: The regulatory mechanisms of the programmed necrosis of cardiomyocytes, that is, the intrinsic (mitochondrial) and extrinsic (death receptor) pathways are summarized and the role of this programmed Necrosis in various heart diseases is also delineated.
Journal ArticleDOI
CaMKII-δ9 promotes cardiomyopathy through disrupting UBE2T-dependent DNA repair.
Mao Zhang,Hua Gao,Dairu Liu,Xiaoming Zhong,Xiaolu Shi,Peng Yu,Li Jin,Yun Liu,Yajie Tang,Yunhu Song,Jinghao Liu,Xinli Hu,Chuan-Yun Li,Lei Song,Jun Qin,Fujian Wu,Feng Lan,Yan Zhang,Rui-Ping Xiao +18 more
TL;DR: The role of CaMKII-δ9, a previously less-studied isoform, in driving cardiomyopathy is reported and is marked as an important therapeutic target for cardiomeopathy and heart failure.