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首页> 外文期刊>Disease Prevention Daily. >Researchers at Shanghai Jiao Tong University School of Medicine Report Research in Sepsis (Mitophagy coordinates the mitochon-drial unfolded protein response to attenuate inflammation-mediated myocardial injury)
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Researchers at Shanghai Jiao Tong University School of Medicine Report Research in Sepsis (Mitophagy coordinates the mitochon-drial unfolded protein response to attenuate inflammation-mediated myocardial injury)

机译:上海交通大学的研究人员医学院的脓毒症的研究报告(Mitophagy坐标mitochon-drial展开的蛋白质反应减弱inflammation-mediated心肌损伤)

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摘要

2021 SEP 07 (NewsRx) - By a News Reporter-Staff News Editor at Disease Prevention Daily - Data detailed on sepsis have been presented. According to news reporting from Shanghai, People's Republic of China, by NewsRx journalists, research stated, "Mitochondrial dysfunction is a fundamental challenge in septic cardiomyopathy. Mitophagy and the mitochondrial unfolded protein response (UPRmt) are the predominant stress-responsive and protective mechanisms involved in repairing damaged mitochondria." Our news journalists obtained a quote from the research from Shanghai Jiao Tong University School of Medicine: "Although mitochondrial homeostasis requires the coordinated actions of mitophagy and UPRmt, their molecular basis and interactive actions are poorly understood in sepsis-induced myocardial injury. Our investigations showed that lipopolysaccharide (LPS)-induced sepsis contributed to cardiac dysfunction and mitochondrial damage. Although both mitophagy and UPRmt were slightly activated by LPS in cardiomyocytes, their endogenous activation failed to prevent sepsis-mediated myocardial injury. However, administration of urolithin A, an inducer of mitophagy, obviously reduced sepsis-mediated cardiac depression by normalizing mitochondrial function. Interestingly, this beneficial action was undetectable in cardiomyocyte-specific FUNDC1 knockout (FUNDC1CKO) mice.
机译:2021年9月07 (NewsRx)——由一个新闻记者在疾病预防每日新闻编辑——数据详细对脓毒症。来自上海的新闻报道,人民中华民国,NewsRx记者,研究指出:“线粒体功能障碍是一个在脓毒性心肌病根本的挑战。Mitophagy和线粒体的蛋白响应(UPRmt)是主要的逆境应答和保护机制参与修复受损的线粒体。”新闻记者获得的报价上海交通大学的研究医学院的:“尽管线粒体体内平衡需要的协调行动mitophagy UPRmt,其分子基础和互动行为是知之甚少sepsis-induced心肌损伤。调查显示,脂多糖(有限合伙人)全身败血症导致心脏功能障碍和线粒体损伤。mitophagy和UPRmt略激活有限合伙人在心肌细胞,它们的内生防止sepsis-mediated激活失败心肌损伤。很明显,urolithin, mitophagy的诱导物减少sepsis-mediated心脏抑郁线粒体功能正常化。有趣的是,这种有益的行动察觉在cardiomyocyte-specific FUNDC1敲除小鼠(FUNDC1CKO)。

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