ArticleiScience2025
5-HT promotes bronchopulmonary dysplasia via TGM2-mediated serotonylation.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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10 authors.
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Abstract
Bronchopulmonary dysplasia (BPD) is a common chronic lung disease in preterm neonates. Untargeted metabolomics of serum samples revealed that tryptophan metabolism may be involved in the pathogenesis of BPD. Specifically, the serum level of 5-hydroxytryptamine (5-HT), a metabolite of tryptophan, is increased in preterm infants with BPD. Similarly, the pulmonary level of 5-HT is increased in a mouse model of hyperoxia-induced BPD. Administration of 5-HT directly impaired lung maturation. Tryptophan hydroxylase 1 (TPH1) is the rate-limiting enzyme in the biosynthesis of 5-HT. As expected, the TPH1 inhibitor LP533401 mitigated lung injury in pups exposed to 85% oxygen. Mechanistically, 5-HT promotes post-translational serotonylation via transglutaminase 2 (TGM2) in alveolar epithelial cells. TGM2 expression is increased in the pulmonary tissues of BPD-like mice. Blocking TGM2 partially reversed BPD-like damage to the lungs. Collectively, our findings highlight the roles of 5-HT and serotonylation in the pathogenesis of BPD.
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