ArticleFrontiers in immunology2026
Upregulation of Trx alleviated high-glucose-induced Müller cell pyroptosis through ASK-1/Cav-1-mediated endoplasmic reticulum stress and autophagy.
Article in Frontiers in immunology, 2026. 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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Abstract
Objectives: Diabetic retinopathy (DR) is a vision-threatening complication of diabetes. A high-glucose state induces endoplasmic reticulum stress (ERS) and autophagy in retinal Müller cells and further triggers pyroptosis, which ultimately promotes the progression of DR. Apoptosis signal-regulating kinase 1 (ASK1) and caveolin-1 (Cav-1) have been found to be closely associated with ERS and autophagy. Thioredoxin (Trx), a small-molecule protein, is essential for regulating cellular function. However, the regulatory mechanisms linking these molecules are not fully understood in DR. In this study, we investigated the role and mechanism of Trx in alleviating high-glucose-induced pyroptosis in Müller cells. Study design: Serum samples from patients with diabetes, diabetic mice, and Müller cells were used in the study. Results: Conclusions: Trx overexpression could delay high-glucose-induced Müller cell pyroptosis by regulating ERS and autophagy via ASK-1/Cav-1, providing a new therapeutic target for DR treatment.
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