| Literature DB >> 33511136 |
Daniela Ramaccini1,2,3, Vanessa Montoya-Uribe1, Femke J Aan1, Lorenzo Modesti2,3, Yaiza Potes4, Mariusz R Wieckowski4, Irena Krga5, Marija Glibetić5, Paolo Pinton2,3,6, Carlotta Giorgi2,3, Michelle L Matter1.
Abstract
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. Ca2+ 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.Entities:
Keywords: Ca ATPase (SERCA) 2+; calcium; cardiomyocytes; cardiomyopathies; heart function; mitochondria; organoids model; sarcoplasmic reticulum
Year: 2021 PMID: 33511136 PMCID: PMC7835522 DOI: 10.3389/fcell.2020.624216
Source DB: PubMed Journal: Front Cell Dev Biol ISSN: 2296-634X