ArticleJournal of translational medicine2025
LOX-induced tubulointerstitial fibrosis via the TGF-β/LOX/Snail axis in diabetic mice.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Bibliometric analysis combined with visualization on universal trends and hot topics of LOX family in human diseases: 1995 to 2025.Frontiers in oncology · 2025Pooled it
- Lysyl oxidase (LOX) family proteins in extracellular matrix homeostasis: roles in disease and radiation-induced pathogenesis.Molecular biology reports · 2026Review
- Oxidative Stress-Induced Expression Levels of PXDN and NF-κB in Type 2 Diabetic Patients With Nephropathy.Endocrinology, diabetes & metabolism · 2026Article
- Expression of Lysyl Oxidase-Related Protein and Effect of Lysyl Oxidase Inhibition in Cyclosporine-Induced Nephropathy Mouse Model.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Molecular mechanisms and novel therapeutic targets of diabetic kidney disease.Chinese medical journal · 2026Review
- Mossy-textured hydroxyapatite-modified poly (lactic-co-glycolic acid) microspheres promote collagen regeneration via calcium/TGF-β and chemokine signaling pathways in soft tissue augmentation.Bioactive materials · 2026Article
- CILP2: From ECM Component to a Pleiotropic Modulator in Metabolic Dysfunction, Cancer, and Beyond.Biomolecules · 2026Review
- Article
- GPR4 promotes immune exclusion in colon cancer through LOXL2-mediated extracellular matrix remodeling.Nature communications · 2025Article
- Tracing the molecular landscape of diabetic nephropathy: Insights from machine learning and experiment verification.Journal of diabetes investigation · 2025Article
- Systematic Characterisation and Analysis of Lysyl Oxidase Family Members as Drivers of Tumour Progression and Multiple Drug Resistance.Journal of cellular and molecular medicine · 2025Article
- MTHFD2 stabilizes LOX expression through RNA methylation modification to promote sepsis-induced acute kidney injury progression.Human cell · 2025Article
- Research progress of copper in diabetes and diabetic kidney disease: a narrative review.Frontiers in endocrinology · 2025Review
- The Function of the TGFβ Signaling Pathway in Connective Tissue Diseases: From Biology to Clinical Application.Journal of inflammation research · 2025Review
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5 authors.
Funding
Abstract
backgroundThe partial epithelial-mesenchymal transition (EMT) is emerging as a significant mechanism in diabetic nephropathy (DN). LOX is a copper amine oxidase conventionally thought to act by crosslinking collagen. However, the role of LOX in partial EMT and fibrotic progression in diabetic nephropathy has not been investigated experimentally.
methodsThe bulk RNA sequencing and single-nuclei RNA sequencing (snRNA-seq) analysis were explored to find the role of LOX in diabetic nephropathy. We then investigated the partial EMT and the possible signaling pathway of LOX, both in vivo and in vitro by LOX inhibition experiments in diabetic mice and HK-2 cells. Besides, we further assessed kidney fibrosis and renal function.
resultsLOX expression was elevated in kidneys of diabetic mice. Additionally, snRNA-seq results indicated that LOX expression was higher in partial epithelial-mesenchymal transition proximal tubular (PemtPT) epithelial cells. Moreover, we found that increased LOX prompted partial EMT of renal tubular epithelial cells (RTECs) by modulating the transcription factor Snail both in vivo and in vitro. Remarkably, inhibition of LOX effectively mitigated the partial EMT of RTECs in diabetic mice, thereby attenuating kidney fibrosis and enhancing renal function. Additionally, we identified the TGF-β signaling pathway as an upstream regulator of LOX, and inhibiting LOX partially reversed the partial EMT program in HK-2 cells induced by the TGF-β signaling pathway.
conclusionsHyperglycemia induces partial EMT of RTECs via the TGF-β/LOX/Snail axis, thereby contributing to diabetic kidney fibrosis. Inhibiting LOX can effectively reverse the partial EMT of RTECs, diminish diabetic kidney fibrosis, and improve renal function.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.