Cited by 48Mitochondrial Function and PathologyCardiac Ischemia and ReperfusionAutophagy in Disease and Therapy

[Retracted] Mitochondrial Dysfunction and Cardiovascular Disease: Pathophysiology and Emerging Therapies

Open access
Stamerra, Cosimo Andrea, Di Giosia, Paolo, Giorgini, Paolo, Ferri, Claudio, Sukhorukov, Vasily N., Sahebkar, Amirhossein·2022·Oxidative Medicine and Cellular Longevity

Abstract

Mitochondria ensure the supply of cellular energy through the production of ATP via oxidative phosphorylation. The alteration of this process, called mitochondrial dysfunction, leads to a reduction in ATP and an increase in the production of reactive oxygen species (ROS). Mitochondrial dysfunction can be caused by mitochondrial/nuclear DNA mutations, or it can be secondary to pathological conditions such as cardiovascular disease, aging, and environmental stress. The use of therapies aimed at the prevention/correction of mitochondrial dysfunction, in the context of the specific treatment of cardiovascular diseases, is a topic of growing interest. In this context, the data are conflicting since preclinical studies are numerous, but there are no large randomized studies.

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Crossref · 10.1155/2022/9530007This paper is marked retracted.

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  • Mitochondrial function is widely recognized as a factor in the pathophysiology of several psychiatric disorders, including MDD, and a variety of physical conditions, such as metabolic diseases, cardiovascular diseases, and neurodegenerative disorders.

    “Mitochondrial function is widely recognized as a factor in the pathophysiology of several psychiatric disorders, including MDD216, and a variety of physical conditions, such as metabolic diseases217, cardiovascular diseases218, and neurodegenerative disorders219.”

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Authors
Stamerra, C. A., Di Giosia, P., Giorgini, P., Ferri, C., Sukhorukov, V. N., & Sahebkar, A.
Affiliations
  • University of L'Aquila (IT)
  • Institute for Atherosclerosis Research (RU)
  • Mashhad University of Medical Sciences (IR)
Corresponding author
Sahebkar, Amirhossein
Venue
Oxidative Medicine and Cellular Longevity
Publisher
Wiley
Published
2022-01
Volume
2022
Issue
1
Pages
9530007-9530007
ISSN
  • 1942-0994 (ISSN-L)
  • 1942-0900
OpenAlex
W4289519687
Cited by
48
References
238
Citations by year
2026: 5 · 2025: 7 · 2024: 20 · 2023: 14 · 2022: 2
FWCI
3.51
Type
journal article
Language
en
Status
Retracted
Open access
Locations
  • Oxidative Medicine and Cellular Longevity (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
  • Archivio Istituzionale della Ricerca - Università degli Studi dell Aquila (submittedVersion)
Funders
Russian Science Foundation (22-15-00064)
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, cardiovascular disease, oxidative phosphorylation, ATP production, reactive oxygen species, mitochondrial DNA mutations, nuclear DNA mutations, aging, environmental stress, mitochondrial-targeted therapy
MeSH terms
Adenosine Triphosphate, Cardiovascular Diseases, DNA, Mitochondrial, Humans, Mitochondria, Oxidative Phosphorylation, Reactive Oxygen Species, Oxidative Stress

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