Mitochondria as Therapeutic Targets in Heart Failure.
Cardiac metabolism
Elamipretide
Heart failure
MitoQ
Mitochondria
Reactive oxygen species
SGLT2 inhibitors
Journal
Current heart failure reports
ISSN: 1546-9549
Titre abrégé: Curr Heart Fail Rep
Pays: United States
ID NLM: 101196487
Informations de publication
Date de publication:
04 2022
04 2022
Historique:
accepted:
12
01
2022
pubmed:
12
2
2022
medline:
26
4
2022
entrez:
11
2
2022
Statut:
ppublish
Résumé
We review therapeutic approaches aimed at restoring function of the failing heart by targeting mitochondrial reactive oxygen species (ROS), ion handling, and substrate utilization for adenosine triphosphate (ATP) production. Mitochondria-targeted therapies have been tested in animal models of and humans with heart failure (HF). Cardiac benefits of sodium/glucose cotransporter 2 inhibitors might be partly explained by their effects on ion handling and metabolism of cardiac myocytes. The large energy requirements of the heart are met by oxidative phosphorylation in mitochondria, which is tightly regulated by the turnover of ATP that fuels cardiac contraction and relaxation. In heart failure (HF), this mechano-energetic coupling is disrupted, leading to bioenergetic mismatch and production of ROS that drive the progression of cardiac dysfunction. Furthermore, HF is accompanied by changes in substrate uptake and oxidation that are considered detrimental for mitochondrial oxidative metabolism and negatively affect cardiac efficiency. Mitochondria lie at the crossroads of metabolic and energetic dysfunction in HF and represent ideal therapeutic targets.
Identifiants
pubmed: 35147851
doi: 10.1007/s11897-022-00539-0
pii: 10.1007/s11897-022-00539-0
pmc: PMC9023431
doi:
Substances chimiques
Reactive Oxygen Species
0
Adenosine Triphosphate
8L70Q75FXE
Types de publication
Journal Article
Review
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
27-37Informations de copyright
© 2022. The Author(s).
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