TY  - JOUR
A1  - Bețiu, Alina M.
A1  - Noveanu, Lavinia
A1  - Hâncu, Iasmina M.
A1  - Lascu, Ana
A1  - Petrescu, Lucian
A1  - Maack, Christoph
A1  - Elmér, Eskil
A1  - Muntean, Danina M.
T1  - Mitochondrial effects of common cardiovascular medications: the good, the bad and the mixed
JF  - International Journal of Molecular Sciences
N2  - 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.
KW  - cardiovascular drugs
KW  - drug toxicity
KW  - mitochondria function and morphology
KW  - adverse effects
KW  - lactic acidosis
KW  - drug intoxication
KW  - drug interaction
Y1  - 2022
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-297384
SN  - 1422-0067
VL  - 23
IS  - 21
ER  -