Researchers identified three mechanistically distinct compounds that prevent cellular senescence in developing human airway smooth muscle cells exposed to moderate hyperoxia (50% oxygen). Fucoidan at 100 μg/mL acted as a senomorphic, reducing p21 expression and inflammatory secretions without killing cells. The senolytic combination dasatinib plus quercetin (250 nM + 375 nM) decreased senescence markers and induced targeted cell death of damaged cells. MitoQ at 100 nM prevented senescence onset when used prophylactically, functioning as a mitochondrial antioxidant. This work advances our understanding of how supplemental oxygen therapy—commonly used in neonatal intensive care—may inadvertently accelerate cellular aging in developing lungs. The finding that even moderate oxygen levels (50% versus normal 21%) trigger senescence pathways suggests current clinical practices may need refinement. Each therapeutic approach offers distinct advantages: senomorphics maintain cell populations while reducing harm, senolytics eliminate damaged cells, and antioxidants prevent damage entirely. While promising, these are early-stage cell culture findings that require extensive safety testing before clinical application, particularly given the vulnerable patient population of premature infants.