TY  - JOUR
A1  - Schwemmlein, Julia
A1  - Maack, Christoph
A1  - Bertero, Edoardo
T1  - Mitochondria as therapeutic targets in heart failure
T2  - Current Heart Failure Reports
N2  - Purpose of Review
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.

Recent Findings
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.

Summary
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.
KW  - mitochondria
KW  - heart failure
KW  - reactive oxygen species
KW  - MitoQ
KW  - elamipretide
KW  - SGLT2 inhibitors
KW  - cardiac metabolism
Y1  - 2022
UR  - https://opus.bibliothek.uni-wuerzburg.de/frontdoor/index/index/docId/32401
UR  - https://nbn-resolving.org/urn:nbn:de:bvb:20-opus-324015
VL  - 19
IS  - 2
ER  -