Heat-shock transcription factor 1 is critically involved in the ischaemia-induced cardiac hypertrophy via JAK2/STAT3 pathway.

Heat-shock transcription factor 1 is critically involved in the ischaemia-induced cardiac hypertrophy via JAK2/STAT3 pathway. J Cell Mol Med. 2018 Jul 11;: Authors: Yuan L, Qiu L, Ye Y, Wu J, Wang S, Wang X, Zhou N, Zou Y Abstract Cardiac hypertrophy after myocardial infarction (MI) is an independent risk factor for heart failure. Regression of cardiac hypertrophy has emerged as a promising strategy in the treatment of MI patients. Here, we have been suggested that heat-shock transcription factor 1 (HSF1) is a novel repressor of ischaemia-induced cardiac hypertrophy. Ligation of left anterior descending coronary was used to produce MI in HSF1-deficient heterozygote (KO), HSF1 transgenic (TG) mice and their wild-type (WT) littermates, respectively. Neonatal rat cardiomyocytes (NRCMs) were treated by hypoxia to mimic MI in vitro. The HSF1 phosphorylation was significantly reduced in the infarct border zone of mouse left ventricles (LVs) 1 week after MI and in the hypoxia-treated NRCMs. HSF1 KO mice showed more significant maladaptive cardiac hypertrophy and deteriorated cardiac dysfunction 1 week after MI compared to WT MI mice. Deficiency of HSF1 by siRNA transfection notably increased the hypoxia-induced myocardial hypertrophy in NRCMs. Mechanistically, Janus kinase 2 (JAK2) and its effector, signal transducer and activator of transcription 3 (STAT3) were found to be significantly increased in the LV infarct border zone of WT mice after MI as well as the...
Source: J Cell Mol Med - Category: Molecular Biology Authors: Tags: J Cell Mol Med Source Type: research

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The Hospital Readmissions Reduction Program (HRRP) has been associated with substantial reductions in readmission within 30 days of discharge among fee-for-service Medicare beneficiaries aged ≥65 years who are hospitalized with acute myocardial infarction, heart failure, or pneumonia – the target population for this program.1,2 There have been suggestions that hospitals may have pursued reductions in readmissions through efforts mainly directed towards Medicare beneficiaries aged ≥ 65 years without pursuing systematic improvements in the care of patients.
Source: The American Journal of Medicine - Category: General Medicine Authors: Tags: Clinical Research Study Source Type: research
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Source: Medical Care - Category: Health Management Tags: Original Articles Source Type: research
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Source: Medical Care - Category: Health Management Tags: Original Articles Source Type: research
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Source: Redox Biology - Category: Biology Source Type: research
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Source: Clinica Chimica Acta - Category: Laboratory Medicine Source Type: research
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