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Understanding how O\n                    <jats:sub>2<\/jats:sub>\n                    exposure drives long-term bronchial changes in prematurity is critical for developing therapies for airway disease across the lifespan. Premature lungs have immature antioxidant defenses, potentially due to disrupted mitochondrial dynamics, increasing susceptibility to O\n                    <jats:sub>2<\/jats:sub>\n                    -induced oxidative stress. Thus, mitochondrial homeostasis is highly relevant to ASM dysfunction and airway disease. We propose that hyperoxia in prematurity promotes mitochondrial dysfunction, and that the gasotransmitter hydrogen sulfide (H\n                    <jats:sub>2<\/jats:sub>\n                    S) mitigates O\n                    <jats:sub>2<\/jats:sub>\n                    -induced mitochondrial damage in developing ASM. Human fetal ASM (fASM) cells were exposed to moderate hyperoxia to investigate the effects of exogenous H\n                    <jats:sub>2<\/jats:sub>\n                    S donors (GYY4137, AP39) and stabilization of cystathionine \u03b2-synthase (CBS), an H\n                    <jats:sub>2<\/jats:sub>\n                    S biosynthetic enzyme, on mitochondrial structure and function. Hyperoxia impaired fASM cell mitochondrial integrity, while H\n                    <jats:sub>2<\/jats:sub>\n                    S donors in particular, or CBS stabilization attenuated adverse O\n                    <jats:sub>2<\/jats:sub>\n                    effects on mitochondrial morphology, ROS, respiration, calcium regulation, and contractility. These findings highlight the therapeutic potential of H\n                    <jats:sub>2<\/jats:sub>\n                    S in the premature lung exposed to moderate hyperoxia.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.191475","type":"journal-article","created":{"date-parts":[[2026,3,10]],"date-time":"2026-03-10T16:00:22Z","timestamp":1773158422000},"source":"Crossref","is-referenced-by-count":1,"title":["Hydrogen sulfide alleviates hyperoxia effects on mitochondria in human developing airway smooth muscle"],"prefix":"10.1172","volume":"11","author":[{"given":"Colleen M.","family":"Bartman","sequence":"first","affiliation":[{"name":"Department of Anesthesiology and Perioperative Medicine, Mayo Clinic, Rochester, Minnesota, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"Thompson","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology and Perioperative Medicine, Mayo Clinic, Rochester, Minnesota, 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