ArticleArchives of medical science : AMS2024
Lysozyme promotes renal fibrosis through the JAK/STAT3 signal pathway in diabetic nephropathy.
Article in Archives of medical science : AMS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 11 citations in OpenAlex.
- Overexpression of LINC00472 alleviates diabetic kidney disease progression via the miR-21-5p/STAT3 axis.Renal failure · 2026Article
- The landscape of allele-specific expression in human kidneys.Science advances · 2026Article
- Polymeric alpha-1 antitrypsin perturbs Paneth cell proteostasis and exacerbates intestinal inflammation.Signal transduction and targeted therapy · 2026Article
- Proteomic risk score for early prediction of kidney disease progression in individuals with APOL1 high-risk genotypes.Nature medicine · 2026Article
- Multi-omics and machine learning reveal LYZ and ISG15 as diagnostic and therapeutic targets in autoimmune-mediated chronic kidney disease.Frontiers in immunology · 2026Article
- Immunomodulatory Functions of Intercalated Cells in Kidney Autoimmunity.bioRxiv : the preprint server for biology · 2025Article
- The geroprotectors trametinib and rapamycin combine additively to extend mouse healthspan and lifespan.Nature aging · 2025Article
- Decoding diabetic kidney disease: a comprehensive review of interconnected pathways, molecular mediators, and therapeutic insights.Diabetology & metabolic syndrome · 2025Review
- Spatial transcriptomics reveals prognostically LYZCancer immunology, immunotherapy : CII · 2025Article
- Mesenchymal stem cells suppress kidney injury molecule-1 associated with inhibition of renal PKC/NF-Kβ/STAT3 fibrotic signaling pathway in rats with diabetic nephropathy.Archives of medical science : AMS · 2025Article
- Integrated multi-omics for potential biomarkers and molecular mechanism of persistent inflammatory refractory rheumatoid arthritis.Frontiers in immunology · 2025Article
- Ursolic Acid Ameliorates Diabetic Nephropathy by Inhibiting JAK2/STAT3-Driven Ferroptosis: Mechanistic Insights from Network Pharmacology and Experimental Validation.Drug design, development and therapy · 2025Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Diabetic nephropathy (DN) is a leading cause of kidney failure. Lysozyme (LYZ) is an essential component of innate immunity and exhibits antibacterial properties. However, LYZ has been reported to induce nephropathy, implying a possible association between impaired renal function and lysozyme expression. Material and methods: Bioinformatics analysis was used to predict the hub gene associated with DN, and the differential expression of the hub gene was confirmed using a mouse model. A mouse model of streptozotocin (STZ)-induced diabetic nephropathy was established to investigate the correlation between DN and LYZ expression, and the functionality of LYZ was verified through knockdown and overexpression experiments conducted Results: Mechanistically, 25 mM glucose promotes the expression of LYZ in fibroblastic cells, and LYZ may in turn promote the proliferation of renal interstitial fibroblasts. Western blot shows that glucose can activate STAT3 in an LYZ-dependent manner, and the JAK inhibitor AG490 can partially suppress LYZ-induced STAT3 activation. Furthermore, Conclusions: Lysozyme promotes kidney fibrosis via the JAK/STAT3 signaling pathway in diabetic nephropathy, and glucose may promote fibroblast proliferation by promoting LYZ auto-secretion.
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