ArticleAmerican journal of physiology. Cell physiology2026
Computational modeling of substrate-dependent lung mitochondrial respiration and bioenergetics in rats with different susceptibility to hyperoxia-induced ARDS.
Article in American journal of physiology. Cell physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Prolonged exposure to high oxygen levels (hyperoxia) is unavoidable in managing severe acute respiratory distress syndrome (ARDS), but can itself worsen lung injury and increase mortality. Rats conditioned to be hyperoxia-tolerant (H-T) or hyperoxia-susceptible (H-S) provide a system for assessing the contribution of mitochondrial bioenergetics to the differential susceptibility to hyperoxia-induced ARDS and for identifying potential therapeutic targets. Due to the system's complexity, interpreting lung mitochondrial bioenergetics data from these rat models requires a computational model to define which processes are altered and how changes influence overall lung tissue bioenergetics. We developed a thermodynamically constrained computational model of lung mitochondrial bioenergetics that extends prior models by incorporating regulation by ions (Ca
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