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Full-Text Articles in Medicine and Health Sciences
S100a8/A9 As A Prognostic Biomarker With Causal Effects For Post-Acute Myocardial Infarction Heart Failure, Jie Ma, Yang Li, Ping Li, Xinying Yang, Shuolin Zhu, Ke Ma, Fei Gao, Hai Gao, Hui Zhang, Xin-Liang Ma, Jie Du, Yulin Li
S100a8/A9 As A Prognostic Biomarker With Causal Effects For Post-Acute Myocardial Infarction Heart Failure, Jie Ma, Yang Li, Ping Li, Xinying Yang, Shuolin Zhu, Ke Ma, Fei Gao, Hai Gao, Hui Zhang, Xin-Liang Ma, Jie Du, Yulin Li
Department of Emergency Medicine Faculty Papers
Heart failure is the prevalent complication of acute myocardial infarction. We aim to identify a biomarker for heart failure post-acute myocardial infarction. This observational study includes 1062 and 1043 patients with acute myocardial infarction in the discovery and validation cohorts, respectively. The outcomes are in-hospital and long-term heart failure events. S100A8/A9 is screened out through proteomic analysis, and elevated circulating S100A8/A9 is independently associated with heart failure in discovery and validation cohorts. Furthermore, the predictive value of S100A8/A9 is superior to the traditional biomarkers, and the addition of S100A8/A9 improves the risk estimation using traditional risk factors. We finally report …
Mir15a/Mir16-1 Cluster And Its Novel Targeting Molecules Negatively Regulate Cardiac Hypertrophy., Hongchang Guo, Ke Ma, Wenjing Hao, Yao Jiao, Ping Li, Jing Chen, Chen Xu, Fu-Jian Xu, Wayne Bond Lau, Jie Du, Xin-Liang Ma, Yulin Li
Mir15a/Mir16-1 Cluster And Its Novel Targeting Molecules Negatively Regulate Cardiac Hypertrophy., Hongchang Guo, Ke Ma, Wenjing Hao, Yao Jiao, Ping Li, Jing Chen, Chen Xu, Fu-Jian Xu, Wayne Bond Lau, Jie Du, Xin-Liang Ma, Yulin Li
Department of Emergency Medicine Faculty Papers
In response to pathological stimuli, the heart develops ventricular hypertrophy that progressively decompensates and leads to heart failure. miRNAs are increasingly recognized as pathogenic factors, clinically relevant biomarkers, and potential therapeutic targets. We identified that mir15a/mir16-1 cluster was negatively correlated with hypertrophic severity in patients with hypertrophic cardiomyopathy. The mir15a/mir16-1 expression was enriched in cardiomyocytes (CMs), decreased in hypertrophic human hearts, and decreased in mouse hearts after transverse aortic constriction (TAC). CM-specific mir15a/mir16-1 knockout promoted cardiac hypertrophy and dysfunction after TAC. CCAAT/enhancer binding protein (C/EBP)β was responsible for the downregulation of mir15a/mir16-1 cluster transcription. Mechanistically, mir15a/mir16-1 cluster attenuated the insulin/IGF1 …