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Precision Medicine
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DOI：10.1016/j.jacbts.2025.101345.png)
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Abstract
En 中文
• Maladaptive mitochondrial respiratory alterations and oxidative stress are key contributors to the progression of heart failure. • This review explores mitoprotective therapeutic strategies that have been developed to treat heart failure in both preclinical and clinical settings. • The development of mitochondrial-targeted therapeutics is still in its early stages, with additional preclinical studies required to aid clinical translation.
Keywords:
cardiomyopathy
drug discovery
myocardial metabolism
oxidative stress
respiration
pharmacotherapy
AP39
10-oxo-10-[4-(3-thioxo-3H-1,2-dithiol-5-yl) phenoxy]decyl]triphenyl-phosphonium
ATP
adenosine triphosphate
DNP
2,4-dinitrophenol
dTPP
dodecyl-triphenylphosphonium
eNOS
endothelial nitric oxidase synthase
HCM
hypertrophic cardiomyopathy
HF
heart failure
HFpEF
heart failure with preserved ejection fraction
HFrEF
heart failure with reduced ejection fraction
iNOS
inducible nitric oxidase synthase
LV
left ventricle
MitoQ
mitoquinone mesylate
Mito Tempol
4-(1-hydroxy-2,2,6,6-tetramethylpiperidin-4-yl) oxybutyl-triphenylphosphonium
MRA
mineralocorticoid receptor antagonist
mtDNA
mitochondrial DNA
NOS
nitric oxidase synthase
PCr
phosphocreatine
RAAS
renin-angiotensin-aldosterone system
ROS
reactive oxygen species
SkQ1
10-(6'-plastoquinonyl) decyltriphenylphosphonium
SOD
superoxide dismutase
SS31
Szeto–Schiller 31
XO
xanthine oxidase
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