Ramaccini Daniela, Montoya-Uribe Vanessa, Aan Femke J, Modesti Lorenzo, Potes Yaiza, Wieckowski Mariusz R, Krga Irena, Glibetić Marija, Pinton Paolo, Giorgi Carlotta, Matter Michelle L
University of Hawaii Cancer Center, Honolulu, HI, United States.
Department of Medical Sciences, University of Ferrara, Ferrara, Italy.
Front Cell Dev Biol. 2021 Jan 12;8:624216. doi: 10.3389/fcell.2020.624216. eCollection 2020.
Cardiac tissue requires a persistent production of energy in order to exert its pumping function. Therefore, the maintenance of this function relies on mitochondria that represent the "powerhouse" of all cardiac activities. Mitochondria being one of the key players for the proper functioning of the mammalian heart suggests continual regulation and organization. Mitochondria adapt to cellular energy demands via fusion-fission events and, as a proof-reading ability, undergo mitophagy in cases of abnormalities. Ca fluxes play a pivotal role in regulating all mitochondrial functions, including ATP production, metabolism, oxidative stress balance and apoptosis. Communication between mitochondria and others organelles, especially the sarcoplasmic reticulum is required for optimal function. Consequently, abnormal mitochondrial activity results in decreased energy production leading to pathological conditions. In this review, we will describe how mitochondrial function or dysfunction impacts cardiac activities and the development of dilated cardiomyopathy.
心脏组织需要持续产生能量以发挥其泵血功能。因此,这种功能的维持依赖于线粒体,线粒体是所有心脏活动的“动力源”。线粒体是哺乳动物心脏正常运作的关键因素之一,这表明需要持续的调节和组织。线粒体通过融合-分裂事件适应细胞能量需求,并作为一种校对能力,在出现异常时进行线粒体自噬。钙通量在调节所有线粒体功能中起关键作用,包括ATP产生、代谢、氧化应激平衡和细胞凋亡。线粒体与其他细胞器,尤其是肌浆网之间的通讯对于最佳功能是必需的。因此,线粒体活性异常会导致能量产生减少,从而引发病理状况。在本综述中,我们将描述线粒体功能正常或异常如何影响心脏活动以及扩张型心肌病的发展。