[Retracted] Mitochondrial Dysfunction and Cardiovascular Disease: Pathophysiology and Emerging Therapies
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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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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.”
From Comorbidity between major depressive disorder and physical diseases: a comprehensive review of epidemiology, mechanisms and management (2023) · cites this paper as [218]
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Flagged first, then by citations
Cited by
Sorted by citations
Berk, M., Köhler‐Forsberg, O., Turner, M., Penninx, B. W. J. H., Wrobel, A., Firth, J., Loughman, A., Reavley, N. J., McGrath, J. J., Momen, N. C., et al. (2023) · World Psychiatry · doi:10.1002/wps.21110 · Cited by 336 · see citing works
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Cellular Senescence, Mitochondrial Dysfunction, and Their Link to Cardiovascular Disease
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“Therefore, restoring their ATP-producing capacity and counteracting the damaging effects of ROS to reduce oxidative stress and chronic inflammation have been suggested as primary therapeutic targets to improve mitochondrial dysfunction [31].”
BackgroundMitochondrial dysfunction at the crossroad of cardiovascular diseases and cancer
Rocca, C., Soda, T., Francesco, E. D. D., Fiorillo, M., Moccia, F., Viglietto, G., Angelone, T., & Amodio, N. (2023) · Journal of Translational Medicine · doi:10.1186/s12967-023-04498-5 · Cited by 82 · see citing works
“A crucial determinant of CVDs may also be represented by mtDNA mutations leading to OXPHOS impairment [96].”
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Mitochondrial transplantation as a novel therapeutic strategy for cardiovascular diseases
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“Ultrastructural analysis shows a significant increase in the number and size of mitochondria, resulting in the enlargement of cardiomyocytes and sarcomere disorders hinder contractile activity in mitochondrial heart disease [17].”
BackgroundThe impact of oxidative stress on abnormal lipid metabolism-mediated disease development
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Resveratrol combats chronic diseases through enhancing mitochondrial quality
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“Consequently, this recognition bears significant new implications for the understanding One of the major driving forces of the inflammatory response in ECs is low-density lipoprotein (LDL) in its oxidized form (oxLDL), promoting plaque formation [161–163]. of CVD development [20,73,168].”
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Oxidative Stress Biomarkers in Coronary Artery Disease
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“In addition, mitochondria are the major intracellular source of ROS and are the site of the Krebs cycle that translate the products of the catabolism of carbohydrates, lipids, and proteins into reduced nicotinamide adenine dinucleotide and flavin adenine dinucleotide, which are substrates of the electron transport cha…”
BackgroundDysfunctional mitochondria elicit bioenergetic decline in the aged heart
Mone, P., Agyapong, E. D., Morciano, G., Jankauskas, S. S., Luca, A. D., Varzideh, F., Pinton, P., & Santulli, G. (2024) · The Journal of Cardiovascular Aging · doi:10.20517/jca.2023.50 · Cited by 19 · see citing works
“Hence arises the necessity for the cell to eliminate these dysfunctional organelles in order to preserve cellular homeostasis [165,166] .”
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“Aberrations in mitochondrial function can lead to metabolic disorders and CVDs. Impaired mitochondrial function can cause defective oxidative phosphorylation and abnormally high levels of ROS generation [86, 87].”
The mitochondrial link: Phthalate exposure and cardiovascular disease
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“However, we cannot underestimate the impact of mitochondrial dysfunction and signaling dysregulation in driving proper cardiomyocyte maturation, cardiac differentiation, and heart organogenesis that may only be perceivable in advanced postnatal life stages [49,62,63].”
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Building the case for mitochondrial transplantation as an anti-aging cardiovascular therapy
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Mitochondrial biomarkers for airborne particulate matter–associated cardiovascular diseases
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“…in aging populations [4], and the main four sources widely acknowledged as being responsible for the increased generation of reactive oxygen species (ROS) are NADPH oxidases, a dysfunctional mitochondrial electron transport system, uncoupled endothelial NO synthase and xanthine oxidase [5–9].”
BackgroundAnalyses of mitochondrial metabolism in diseases: a review on 13 C magnetic resonance tracers
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“18 As a highly energy-demanding organ, the heart can be greatly a ff ected by reduced ATP production and impaired cardiac function caused by mitochondrial dysfunction.”
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“The majority of cardiac anomalies are linked to mitochondrial dysfunction that deprives energy and promotes the accumulation of ROS and dysregulation of ionic and metabolic balance [35].”
BackgroundMetabolic and Mitochondrial Myopathies
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“…mitochondrial dysfunction are associated with the development of several age-related chronic conditions, most notably cardiovascular disease (CVD), as the pathophysiology of CVD may be particularly sensitive to oxidative damage and mitochondrial dysfunction impacting calcium homeostasis [11, 12].”
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“Thus, the ATP de fi ciency observed in the traditional view may (68, 69, 75), to a signi fi cant extent, be a downstream consequence of upstream ion pump failure and subsequent calcium overload.”
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“Mitochondria could provide cellular energy for cell growth through the generation of ATP [24, 25].”
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Is salsolinol a friend or foe? Revisiting its roles in neurotoxicity and cellular protection
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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
- PMC
- PMC9363184
- 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
- Update notices
- retraction (2024-01-09)
- Open access
- hybrid
- doi.org
- 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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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