ArticleFrontiers in medicine2025
Inhibition of renin-angiotensin system attenuates type I alveolar epithelial cell necroptosis in rats after hyperbaric hyperoxic exposure.
Article in Frontiers in medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Pharmaceutical therapies for pyroptosis in lung injury.Inflammopharmacology · 2026Review
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8 authors.
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Abstract
Objective: There is evidence showing both necroptosis and activation of renin-angiotensin system (RAS) are involved in the pathogenesis of hyperbaric hyperoxic lung injury (HLI). This study aimed to investigate whether RAS activation can induce lung cell necroptosis and the cell specificity of necroptosis in the lung in case of hyperbaric HLI. Methods: Male SD rats were randomly assigned into control group ( Results: Either valsartan or captopril pre-treatment could inhibit lung edema, improve blood gas (0 h) and lung function (48 h), and reduce pro-inflammatory factors in the lung. In addition, valsartan or captopril pre-treatment could inhibit AGT1 expression and lung cell necroptosis, and type I alveolar epithelial cells (AECs) were the major cell type experiencing necroptosis after hyperbaric hyperoxic exposure. Conclusion: Our study indicates inhibition of RAS can suppress the hyperbaric HLI, which may be, at least partially, related to the inhibition of type I AECs necroptosis. Our findings provide new mechanism for the protective effects of RAS inhibition on hyperbaric HLI.
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