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Mitochondrial network dynamics in pulmonary disease: Bridging the gap between inflammation, oxidative stress, and bioenergetics.
Metabolic reprogramming, oxidative stress, and pulmonary hypertension.
Activation of the mechanosensitive Ca2+ channel TRPV4 induces endothelial barrier permeability via the disruption of mitochondrial bioenergetics.
Complex interplay between autophagy and oxidative stress in the development of pulmonary disease.
TGF-ß1 attenuates mitochondrial bioenergetics in pulmonary arterial endothelial cells via the disruption of carnitine homeostasis.
Complex I dysfunction underlies the glycolytic switch in pulmonary hypertensive smooth muscle cells.