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Cited by 136Mitochondrial Function and PathologyCardiac Ischemia and ReperfusionAutophagy in Disease and Therapy

Mitochondrial Function and Dysfunction in Dilated Cardiomyopathy

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Ramaccini, Daniela, Montoya-Uribe, Vanessa, Aan, Femke J., Modesti, Lorenzo, Potes, Yaiza, Wieckowski, Mariusz R., Krga, Irena, Glibetić, Marija +3 more·2021·Frontiers in Cell and Developmental Biology
DOI 10.3389/fcell.2020.624216PMC PMC7835522
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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. Ca 2+ 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.

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  • The model identified 478 genes whose loss was predicted to shift cardiomyocytes towards dilated cardiomyopathy, which were enriched for pathways involved in muscle contraction and mitochondrial function.

    “The model identified 478 genes whose loss was predicted to shift cardiomyocytes towards dilated cardiomyopathy, which were enriched for pathways involved in muscle contraction38 and mitochondrial39 function.”

    From Transfer learning enables predictions in network biology (2023) · cites this paper as [39]

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Authors
Ramaccini, D., Montoya-Uribe, V., Aan, F. J., Modesti, L., Potes, Y., Wieckowski, M. R., Krga, I., Glibetić, M., Pinton, P., Giorgi, C., & Matter, M. L.
Affiliations
  • University of Ferrara (IT)
  • University of Hawaii Cancer Center (US)
  • Instytut Biologii Doświadczalnej im. Marcelego Nenckiego (PL)
  • University of Belgrade (RS)
Corresponding author
Matter, Michelle L.
ORCID
Venue
Frontiers in Cell and Developmental Biology
Publisher
Frontiers Media SA
Published
2021-01-12
Volume
8
Pages
624216-624216
ISSN
2296-634X (ISSN-L)
DOI
10.3389/fcell.2020.624216
PMC
PMC7835522
OpenAlex
W3120401257
Cited by
136
References
13
Citations by year
2026: 20 · 2025: 28 · 2024: 30 · 2023: 25 · 2022: 27 · 2021: 6
FWCI
2.31
Type
journal article
Language
en
Open access
Licence
Locations
  • Frontiers in Cell and Developmental Biology (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • RIMI (Institute for Medical Research, University of Belgrade) (submittedVersion, cc-by)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • Institutional Research Information System University of Ferrara (University of Ferrara) (submittedVersion, cc-by)
Funders
National Institutes of Health
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
Keywords
mitochondrial dysfunction, dilated cardiomyopathy, mitochondrial fission and fusion, mitophagy, calcium flux, oxidative stress, apoptosis, sarcoplasmic reticulum, myocardial energy metabolism, ATP production

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