ArticleFrontiers in pharmacology2025
5-methoxytryptophan ameliorates renal ischemia/reperfusion injury by alleviating endoplasmic reticulum stress-mediated apoptosis through the Nrf2/HO-1 pathway.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Renoprotection by 5-Methoxytryptophan in Kidney Disease.Biomolecules · 2026Review
- Buspirone attenuates cyclophosphamide-induced renal dysfunction in association with alterations in miR-205/EGLN2, Nrf2, and PERK/ATF4/CHOP signaling.Frontiers in pharmacology · 2026Article
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5 authors.
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Abstract
Background: Renal ischemia/reperfusion (I/R) injury is a prevalent clinical complication characterized by high incidence and mortality rates. The endogenous metabolite, 5-Methoxytryptophan (5-MTP), derived from tryptophan, possesses anti-inflammatory and antioxidant properties. However, its role in renal I/R injury remains unclear. In this study, we investigated whether 5-MTP could protect the kidney from I/R injury by ameliorating endoplasmic reticulum stress (ERS)-mediated apoptosis through the Nrf2/HO-1 pathway. Methods and results: We established models to examine renal I/R injury in C57BL/6J mice with bilateral renal pedicles clamped and HK-2 cells subjected to hypoxia/reoxygenation (H/R). The administration of 5-MTP improved renal tissue damage and kidney dysfunction impairment and reduced inflammation and oxidative stress. Moreover, 5-MTP attenuated ERS and ERS-mediated apoptosis, while upregulating Nrf2 and HO-1 expression. Additionally, Nrf2-deficient mice and cells were used to determine whether the Nrf2/HO-1 pathway was involved in the role of 5-MTP in alleviating ERS-mediated apoptosis. Nrf2 deficiency led to a partial reduction in the suppressive effects of 5-MTP on inflammation, oxidative stress, and ERS-mediated apoptosis. Conclusion: Our findings suggest that 5-MTP alleviates renal I/R injury by inhibiting ERS-related apoptosis via the Nrf2/HO-1 pathway.
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