ArticleThe Journal of biological chemistry2025
PRDX4 mitigates diabetic retinopathy by inhibiting reactive gliosis, apoptosis, ER stress, oxidative stress, and mitochondrial dysfunction in Müller cells.
Article in The Journal of biological chemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Review
- Crosstalk between endoplasmic reticulum stress and mitochondrial homeostasis: A new perspective on ophthalmic disease treatment.Journal of cell communication and signaling · 2026Review
- Eupalinolide B Alleviates Oxidative Stress in LPS-Induced RAW264.7 Macrophages via Covalently Binding to PRDX4.Biomedicines · 2026Article
- "Age is associated with Achilles tendon thickness in older adults: an ultrasound case-control study with intra-observer reliability".Frontiers in physiology · 2026Article
- Single cell transcriptomic analysis reveals pathogenic cell heterogeneity and candidate inflammatory-associated markers in STZ-induced diabetic mouse retina.Frontiers in immunology · 2026Article
- Crosstalk Between Neuronal and Glial Cells in Diabetic Retinopathy: Mechanisms and Implications for Neurodegeneration.Molecular neurobiology · 2025Review
- Ferroptosis in Müller cells under hyperglycemia: mechanisms and therapeutic implications for diabetic retinopathy-associated optic neuroinflammation.International ophthalmology · 2025Review
- Global research trends on endoplasmic reticulum stress in retinal diseases from 2000 to 2024.International ophthalmology · 2025Review
- Review
- Integrative MultiOmics and Machine Learning Reveal Peroxiredoxin 4 as a Critical Hub Governing Mitochondrial Dysfunction and B Cell Differentiation in Periodontitis.Clinical, cosmetic and investigational dentistry · 2025Article
- Upregulation of SQSTM1 Regulates Ferroptosis and Oxidative Stress in Müller Cells of the Diabetic Neural Retina by Modulating ACSL4.Journal of diabetes research · 2025Article
- Identification and Validation of Feature Genes Related to Mitochondrial Dysfunction and Oxidative Stress in Ulcerative Colitis.Journal of inflammation research · 2025Article
- Hhatl Reduces Apoptosis of Müller Cells in Diabetic Retinopathy by Relieving Endoplasmic Reticulum Stress.International journal of endocrinology · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic retinopathy (DR) is a neurovascular complication of diabetes. As a crucial player in the retinal physiology, Müller cells are affected in DR, impairments of Müller cell function lead to retinal malfunctions. Therefore, searching for approaches to mitigate diabetes-induced injury in Müller cells is imperative for delaying DR. Peroxiredoxin 4 (PRDX4), an important endoplasmic reticulum (ER)-resident antioxidant, was explored in this study for its potential protective role against DR. Streptozotocin-induced mouse model of diabetes and high glucose (HG)-induced Müller cells were utilized to assess the impact of PRDX4. Compared with WT mice, PRDX4 knockout exacerbated retinal neurodegeneration, reactive gliosis, cell apoptosis, ER stress, oxidative stress, and mitochondrial dysfunction in diabetic retinas. Knockdown of PRDX4 aggravated HG-induced reactive gliosis, apoptosis, ER stress, oxidative stress, and mitochondrial dysfunction in Müller cells. Conversely, PRDX4 overexpression in Müller cells protected against HG-induced cell damage. Mechanistically, PRDX4 promoted the degradation of dipeptidyl peptidase-4, which is associated with DR in type 1 diabetics, thereby alleviating HG-stimulated Müller cell abnormalities. Our study indicated that PRDX4 is a crucial protective regulator in DR progression via destabilization of dipeptidyl peptidase-4 protein and suggested that enhancement of PRDX4 level may represent a promising approach for treating DR.
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