Key result
Chronic inhibition of mitochondrial complex III with Antimycin A induced sustained increases in right ventricle systolic pressure, perivascular edema, and a metabolic shift toward glycolysis in female rats.
Why the study?
Does chronic inhibition of mitochondrial complex III with Antimycin A induce pulmonary hypertension and metabolic reprogramming in a rat model?
Population
Female Sprague Dawley rats and a human cohort of 41 patients with right heart catheterization-confirmed…
Comparison
Antimycin A 0.35 mg/kg dissolved in 55%… vs Vehicle (55% ethanol/45% 0.9% saline) injection.
Design
Preclinical, Animals were randomized to receive either vehicle or AA…
Follow-up
24 days
Authors
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Mitochondrial inhibition may initiate PAH-like changes in rats; leaves open causal role in human disease.
Does chronic inhibition of mitochondrial complex III with Antimycin A induce pulmonary hypertension and metabolic reprogramming in a rat model?
p-value: p=<0.05
Chronic mitochondrial complex III inhibition induces pulmonary vasoconstriction, perivascular edema, and a glycolytic shift in rats, mimicking PAH pathology, with nitrosative stress correlating with disease severity in human females.
Rafikova et al. (2018) studied Pulmonary arterial hypertension. Antimycin A vs. Vehicle was evaluated on Right ventricle systolic pressure (RVSP) (p=<0.05). Chronic inhibition of mitochondrial complex III with Antimycin A induced sustained increases in right ventricle systolic pressure, perivascular edema, and a metabolic shift toward glycolysis in female rats.
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