Mitochondrial Effects of Common Cardiovascular Medications: The Good, the Bad and the Mixed.
adverse effects
cardiovascular drugs
drug interaction
drug intoxication
drug toxicity
lactic acidosis
mitochondria function and morphology
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
07 Nov 2022
07 Nov 2022
Historique:
received:
11
09
2022
revised:
20
10
2022
accepted:
28
10
2022
entrez:
11
11
2022
pubmed:
12
11
2022
medline:
15
11
2022
Statut:
epublish
Résumé
Mitochondria are central organelles in the homeostasis of the cardiovascular system via the integration of several physiological processes, such as ATP generation via oxidative phosphorylation, synthesis/exchange of metabolites, calcium sequestration, reactive oxygen species (ROS) production/buffering and control of cellular survival/death. Mitochondrial impairment has been widely recognized as a central pathomechanism of almost all cardiovascular diseases, rendering these organelles important therapeutic targets. Mitochondrial dysfunction has been reported to occur in the setting of drug-induced toxicity in several tissues and organs, including the heart. Members of the drug classes currently used in the therapeutics of cardiovascular pathologies have been reported to both support and undermine mitochondrial function. For the latter case, mitochondrial toxicity is the consequence of drug interference (direct or off-target effects) with mitochondrial respiration/energy conversion, DNA replication, ROS production and detoxification, cell death signaling and mitochondrial dynamics. The present narrative review aims to summarize the beneficial and deleterious mitochondrial effects of common cardiovascular medications as described in various experimental models and identify those for which evidence for both types of effects is available in the literature.
Identifiants
pubmed: 36362438
pii: ijms232113653
doi: 10.3390/ijms232113653
pmc: PMC9656474
pii:
doi:
Substances chimiques
Reactive Oxygen Species
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : COST Innovation Grant IG16225 supported by COST (European Cooperation in Science and Technology).
ID : IG16225
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