Cardiomyocyte-specific deficiency of HSPB1 worsens cardiac dysfunction by activating NFκB-mediated leucocyte recruitment after myocardial infarction
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چکیده
منابع مشابه
Cardiomyocyte cell cycle activation improves cardiac function after myocardial infarction.
AIMS Cardiomyocyte loss is a major contributor to the decreased cardiac function observed in diseased hearts. Previous studies have shown that cardiomyocyte-restricted cyclin D2 expression resulted in sustained cell cycle activity following myocardial injury in transgenic (MHC-cycD2) mice. Here, we investigated the effects of this cell cycle activation on cardiac function following myocardial i...
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RATIONALE Syndecan-4 (Syn4), a cell-surface heparan sulfate proteoglycan, has been detected in the infarct region after myocardial infarction (MI), but its functional significance has not been elucidated. OBJECTIVE We examined whether and how Syn4 regulates the cardiac healing process after MI. METHODS AND RESULTS Although the heart in Syn4-deficient (Syn4(-/-)) mice was morphologically and...
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Effects of Doxycycline on Cx43 Distribution and Cardiac Arrhythmia Susceptibility of Rats after Myocardial Infarction Abstract: This study aimed to observe the effects of doxycycline (DOX) on gap junction remodeling after MI and the susceptibility of rats to cardiac arrhythmia. The proximal left anterior descending coronary artery of rats was ligated to establish a myocardial infarction animal...
متن کاملAkt1-mediated skeletal muscle growth attenuates cardiac dysfunction and remodeling after experimental myocardial infarction.
BACKGROUND It is appreciated that aerobic endurance exercise can attenuate unfavorable myocardial remodeling following myocardial infarction. In contrast, little is known about the effects of increasing skeletal muscle mass, typically achieved through resistance training, on this process. Here, we utilized transgenic (TG) mice that can induce the growth of functional skeletal muscle by switchin...
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ژورنال
عنوان ژورنال: Cardiovascular Research
سال: 2018
ISSN: 0008-6363,1755-3245
DOI: 10.1093/cvr/cvy163