Neonatal Hyperoxia Activates Activating Transcription Factor 4 to Stimulate Folate Metabolism and Alveolar Epithelial Type 2 Cell Proliferation

Yee, Min; McDavid, Andrew; Cohen, Ethan David; Huyck, Heidie; Poole, Cory; Altman, Brian J.; Maniscalco, William M.; Deutsch, Gail H.; Pryhuber, Gloria S.; O’Reilly, Michael A.

doi:10.1165/rcmb.2021-0363oc

Cited by 2 publications

(1 citation statement)

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“…Paradoxically, hyperoxia causes vast destruction of gas exchange [ 254 ], oxidative stress/damage, mitochondrial damage, inflammation, impairment of the innate immune response of macrophages to pathogens [ 255 , 256 , 257 , 258 , 259 , 260 ], platelet activation and sequestration in the pulmonary microcirculation [ 261 ], dysregulation of mechanisms controlling cell proliferation [ 262 ], apoptosis, necrosis, pulmonary fibrosis, and increased mortality of mechanically ventilated patients [ 263 , 264 ]. The airways and lungs are more vulnerable to the undesirable effects of hyperoxia because the respiratory system is the main interface for O2 delivery to the body [ 254 ].…”

Section: Oxidative Stress and Inflammation In Hyperoxiamentioning

confidence: 99%

Oxidative Stress and Inflammation in Acute and Chronic Lung Injuries

Bezerra

Lanzetti

Nesi³

et al. 2023

Antioxidants

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Acute and chronic lung injuries are among the leading causes of mortality worldwide. Lung injury can affect several components of the respiratory system, including the airways, parenchyma, and pulmonary vasculature. Although acute and chronic lung injuries represent an enormous economic and clinical burden, currently available therapies primarily focus on alleviating disease symptoms rather than reversing and/or preventing lung pathology. Moreover, some supportive interventions, such as oxygen and mechanical ventilation, can lead to (further) deterioration of lung function and even the development of permanent injuries. Lastly, sepsis, which can originate extrapulmonary or in the respiratory system itself, contributes to many cases of lung-associated deaths. Considering these challenges, we aim to summarize molecular and cellular mechanisms, with a particular focus on airway inflammation and oxidative stress that lead to the characteristic pathophysiology of acute and chronic lung injuries. In addition, we will highlight the limitations of current therapeutic strategies and explore new antioxidant-based drug options that could potentially be effective in managing acute and chronic lung injuries.

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