REFERENCES

1. Gaddy A, Elrggal M, Madariaga H, Kelly A, Lerma E, Colbert GB. Diabetic kidney disease. Dis Mon. 2025;71:101848.

2. Hu H, Liang W, Ding G. Ion homeostasis in diabetic kidney disease. Trends Endocrinol Metab. 2024;35:142-50.

3. Jin H, Kim YA, Lee Y, et al. Identification of genetic variants associated with diabetic kidney disease in multiple Korean cohorts via a genome-wide association study mega-analysis. BMC Med. 2023;21:16.

4. Dwivedi OP, Barreiro K, Käräjämäki A, et al.; iBEAt. Genome-wide mRNA profiling in urinary extracellular vesicles reveals stress gene signature for diabetic kidney disease. iScience. 2023;26:106686.

5. Jiang WJ, Xu CT, Du CL, et al. Tubular epithelial cell-to-macrophage communication forms a negative feedback loop via extracellular vesicle transfer to promote renal inflammation and apoptosis in diabetic nephropathy. Theranostics. 2022;12:324-39.

6. Zhang JQ, Li YY, Zhang XY, et al. Cellular senescence of renal tubular epithelial cells in renal fibrosis. Front Endocrinol. 2023;14:1085605.

7. Guo M, He F, Zhang C. Molecular therapeutics for diabetic kidney disease: an update. Int J Mol Sci. 2024;25:10051.

8. Wang N, Zhang C. Oxidative stress: a culprit in the progression of diabetic kidney disease. Antioxidants. 2024;13:455.

9. Li L, Fu H, Liu Y. The fibrogenic niche in kidney fibrosis: components and mechanisms. Nat Rev Nephrol. 2022;18:545-57.

10. Chen Y, Zou H, Lu H, Xiang H, Chen S. Research progress of endothelial-mesenchymal transition in diabetic kidney disease. J Cell Mol Med. 2022;26:3313-22.

11. Westra HJ, Peters MJ, Esko T, et al. Systematic identification of trans eQTLs as putative drivers of known disease associations. Nat Genet. 2013;45:1238-43.

12. Sakaue S, Kanai M, Tanigawa Y, et al.; FinnGen. A cross-population atlas of genetic associations for 220 human phenotypes. Nat Genet. 2021;53:1415-24.

13. Emdin CA, Khera AV, Kathiresan S. Mendelian randomization. JAMA. 2017;318:1925-6.

14. Giambartolomei C, Vukcevic D, Schadt EE, et al. Bayesian test for colocalisation between pairs of genetic association studies using summary statistics. PLoS Genet. 2014;10:e1004383.

15. Wang H, Fang F, Zhang M, et al. Nuclear receptor 4A1 ameliorates renal fibrosis by inhibiting vascular endothelial growth factor A induced angiogenesis in UUO rats. Biochim Biophys Acta Mol Cell Res. 2024;1871:119813.

16. Ragland SA, Criss AK. From bacterial killing to immune modulation: recent insights into the functions of lysozyme. PLoS Pathog. 2017;13:e1006512.

17. Tang SCW, Yiu WH. Innate immunity in diabetic kidney disease. Nat Rev Nephrol. 2020;16:206-22.

18. Ren Y, Yu M, Zheng D, He W, Jin J. Lysozyme promotes renal fibrosis through the JAK/STAT3 signal pathway in diabetic nephropathy. Arch Med Sci. 2023;20:233-47.

19. Tang PM, Nikolic-Paterson DJ, Lan H. Macrophages: versatile players in renal inflammation and fibrosis. Nat Rev Nephrol. 2019;15:144-58.

20. Lee YH, Seo J, Kim M, et al. Urinary mRNA signatures as predictors of renal function decline in patients with biopsy-proven diabetic kidney disease. Front Endocrinol. 2021;12:774436.

21. Mitrofanova A, Merscher S, Fornoni A. Kidney lipid dysmetabolism and lipid droplet accumulation in chronic kidney disease. Nat Rev Nephrol. 2023;19:629-45.

22. Kurooka N, Eguchi J, Wada J. Role of glycosylphosphatidylinositol‐anchored high‐density lipoprotein binding protein 1 in hypertriglyceridemia and diabetes. J Diabetes Investig. 2023;14:1148-56.

23. Folestad E, Mehlem A, Ning FC, et al. Vascular endothelial growth factor B-mediated fatty acid flux in the adipose-kidney axis contributes to lipotoxicity in diabetic kidney disease. Kidney Int. 2025;107:492-507.

24. Wu Y, Cheng S, Gu H, et al. Variants within the LPL gene confer susceptility to diabetic kidney disease and rapid decline in kidney function in Chinese patients with type 2 diabetes. Diabetes Obes Metab. 2023;25:3012-9.

25. Meng X, Nikolic-Paterson DJ, Lan HY. TGF-β: the master regulator of fibrosis. Nat Rev Nephrol. 2016;12:325-38.

26. Kopitar-Jerala N. The role of cystatins in cells of the immune system. FEBS Lett. 2006;580:6295-301.

27. Wang H, Inoue A, Lei Y, Wu H, Hong L, Cheng XW. Cathepsins in the extracellular space: focusing on non-lysosomal proteolytic functions with clinical implications. Cell Signal. 2023;103:110531.

28. Zhou Y, Luo Z, Liao C, et al. MHC class II in renal tubules plays an essential role in renal fibrosis. Cell Mol Immunol. 2021;18:2530-40.

29. Zhang W, Ma L, Zhou Q, Gu T, Zhang X, Xing H. Therapeutic targets for diabetic kidney disease: proteome-wide mendelian randomization and colocalization analyses. Diabetes. 2024;73:618-27.

30. Dou F, Liu Q, Lv S, et al. FN1 and TGFBI are key biomarkers of macrophage immune injury in diabetic kidney disease. Medicine. 2023;102:e35794.

31. Huang H, Tang Q, Li S, Qin Y, Zhu G. TGFBI: a novel therapeutic target for cancer. Int Immunopharmacol. 2024;134:112180.

32. Zhao T, Su Z, Li Y, Zhang X, You Q. Chitinase-3 like-protein-1 function and its role in diseases. Sig Transduct Target Ther. 2020;5:201.

33. Montgomery TA, Xu L, Mason S, et al. Breast regression protein–39/chitinase 3–like 1 promotes renal fibrosis after kidney injury via activation of myofibroblasts. J Am Soc Nephrol. 2017;28:3218-26.

34. John SP, Sun J, Carlson RJ, et al. IFIT1 exerts opposing regulatory effects on the inflammatory and interferon gene programs in LPS-activated human macrophages. Cell Rep. 2018;25:95-106.e6.