Mitochondrial Effects of Common Cardiovascular Medications : The Good, the Bad and the Mixed
Bețiu, Alina M. ; Noveanu, Lavinia ; Hâncu, Iasmina M. ; Lascu, Ana ; Petrescu, Lucian ; Maack, Christoph ; Elmér, Eskil LU
and Muntean, Danina M.
(2022)
In International Journal of Molecular Sciences
23(21).
- Abstract
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... (More)
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.
(Less)
- author
- Bețiu, Alina M.
; Noveanu, Lavinia
; Hâncu, Iasmina M.
; Lascu, Ana
; Petrescu, Lucian
; Maack, Christoph
; Elmér, Eskil
LU
and Muntean, Danina M.
- organization
- publishing date
- 2022-11
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- adverse effects, cardiovascular drugs, drug interaction, drug intoxication, drug toxicity, lactic acidosis, mitochondria function and morphology
- in
- International Journal of Molecular Sciences
- volume
- 23
- issue
- 21
- article number
- 13653
- publisher
- MDPI AG
- external identifiers
-
- pmid:36362438
- scopus:85141621086
- ISSN
- 1661-6596
- DOI
- 10.3390/ijms232113653
- language
- English
- LU publication?
- yes
- id
- 4820aa0b-9a84-45d8-89de-89910456ee5a
- date added to LUP
- 2022-12-01 14:51:23
- date last changed
- 2024-05-02 05:53:06
@article{4820aa0b-9a84-45d8-89de-89910456ee5a,
abstract = {{<p>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.</p>}},
author = {{Bețiu, Alina M. and Noveanu, Lavinia and Hâncu, Iasmina M. and Lascu, Ana and Petrescu, Lucian and Maack, Christoph and Elmér, Eskil and Muntean, Danina M.}},
issn = {{1661-6596}},
keywords = {{adverse effects; cardiovascular drugs; drug interaction; drug intoxication; drug toxicity; lactic acidosis; mitochondria function and morphology}},
language = {{eng}},
number = {{21}},
publisher = {{MDPI AG}},
series = {{International Journal of Molecular Sciences}},
title = {{Mitochondrial Effects of Common Cardiovascular Medications : The Good, the Bad and the Mixed}},
url = {{http://dx.doi.org/10.3390/ijms232113653}},
doi = {{10.3390/ijms232113653}},
volume = {{23}},
year = {{2022}},
}