ArticleRespiratory research2025
MIF/CD74 axis regulates alveolar epithelial type II cell apoptosis, autophagy, and transdifferentiation in bronchopulmonary dysplasia via the TGFβ1/SMAD4 pathway.
Article in Respiratory research, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- The molecular mechanisms of gas signaling molecules in bronchopulmonary dysplasia related lung injury.Frontiers in cell and developmental biology · 2026Review
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4 authors.
Funding
Abstract
backgroundBronchopulmonary dysplasia (BPD) is a prevalent cause of lung injury in premature infants. The migration inhibitory factor (MIF), its receptor CD74, and the TGFβ/Smad signaling cascade play pivotal roles in the regulation of alveolar epithelial type II cells (AECIIs) during lung development. This study investigated whether the MIF/CD74 axis regulates AECIIs by modulating the TGFβ/Smad pathway in BPD. MATERIALS AND
methodsA rat model of BPD induced by intraamniotic LPS-injection and postnatal hyperoxia exposure was treated with various interventions and histopathological changes using hematoxylin and eosin staining. In vitro, AECIIs with CD74 or SMAD4 knockdown or overexpression were treated with LPS. Cell proliferation was assessed using BrdU and MTT assays, mRNA expression levels via RT-qPCR, while protein expression was analyzed using immunofluorescence, western blotting, and ELISA.
resultsOur findings revealed that LPS inhibited AECII proliferation, induced transdifferentiation, apoptosis, autophagy, and upregulated MIF, CD74, TGFβ, and phosphorylated Smad proteins both in vitro and in vivo. MIF supplementation and CD74/SMAD4 overexpression reversed LPS-induced effects by promoting proliferation and reducing transdifferentiation, apoptosis, and autophagy in AECIIs. Conversely, MIF inhibition or CD74/SMAD4 knockdown exacerbated these effects. In vivo, MIF and TGFβ1 counteracted the effects of LPS, whereas LL1 enhanced LPS-induced damage. The TGFβ/Smad pathway mediated the regulatory effects of the MIF/CD74 axis in AECIIs within the BPD context.
conclusionThe MIF/CD74 axis regulates AECII phenotypes in BPD via the TGFβ1/Smad4 pathway, underscoring the potential for targeted therapies against the MIF/CD74 axis and TGFβ/Smad signaling for the prevention and treatment of BPD.
trial registrationNot applicable.
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