ArticleFrontiers in medicine2025
TCF3 downregulation alleviates renal fibrosis via PI3K/Akt/mTOR pathway inhibition and autophagy restoration in diabetic nephropathy.
Article in Frontiers in medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Puerarin alleviates inflammation and promotes osteogenic differentiation in periodontitis: insights from autophagy and Notch signaling pathway.Odontology · 2026Article
- The subcellular localization-dependent dual role of NR4A1 in renal fibrosis: mechanisms and therapeutic perspectives.Frontiers in pharmacology · 2026Review
- Hydroxysafflor Yellow A improves diabetic nephropathy by inhibiting PI3K/AKT/mTOR pathway based on a multidimensional study.Frontiers in medicine · 2026Article
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Authors and funding
9 authors.
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Abstract
Background: Diabetic nephropathy (DN) is characterized by tubular injury and tubulointerstitial fibrosis, leading to progressive renal dysfunction. While dysregulation of autophagy has been linked to DN pathogenesis, the underlying regulatory mechanisms remain incompletely understood. This study aimed to test the hypothesis that transcription factor 3 (TCF3) serves as a critical upstream regulator of autophagy dysfunction in DN by suppressing Netrin-1 expression, thereby promoting epithelial-mesenchymal transition (EMT) through activation of the PI3K/Akt/mTOR pathway. Methods: We established a DN rat model using high-fat diet followed by low-dose streptozotocin injection (25 mg/kg). Thirty-five male Sprague-Dawley rats were divided into five groups ( Results: We first confirmed that TCF3 expression was significantly elevated in both DN rat kidneys (2.8-fold increase at protein level, Conclusion: Our findings demonstrate that TCF3 functions as a critical negative regulator of autophagy in DN, establishing a novel TCF3-Netrin-1-autophagy regulatory axis. This study provides new mechanistic insights distinct from previous work by demonstrating the direct transcriptional repression of Netrin-1 by TCF3 in renal pathophysiology. The limitation of our study includes the lack of human DN tissue validation and TCF3-specific pharmacological inhibitors. These findings suggest TCF3 as a potential therapeutic target for preventing renal fibrosis in DN through restoration of autophagy function.
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