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The goal of this study is to learn about CXCL3 as a biomarker for type 2 diabetic kidney disease (DKD) in adults between age of 18-80. The main question it aims to answer is:
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Diabetic kidney disease ( DKD ) has become the first cause of end-stage renal disease. The high cost of treatment brings a heavy burden to the social economy and medical insurance. However, the pathogenesis of DKD is still unclear. Because the early symptoms of DKD are hidden and difficult to diagnose, once a large amount of proteinuria occurs in clinical practice, renal damage is often difficult to reverse, and patients will soon enter ESRD. Therefore, it is of great social significance and economic benefits to clarify the pathogenesis of DKD and find more effective therapeutic targets for DKD.In our previous bioinformatics analysis, it was found that CXCL3 was significantly increased in peripheral blood PBMC of DKD, and CXCL3 was the core gene of DKD after screening by WGCNA and machine learning. CXC legend 3 ( CXCL3 ), also known as GRO gamma ( GROγ ), is a 7.9 kDa protein composed of 73 amino acids. CXCL3 is a member of the CXC subfamily of chemokines, including the ' ELR ' motif of its receptor CXCR2 tuberculosis. CXCL3 is considered to be a chemotactic factor for neutrophils, while CXCL3 has other proven roles in the field of cancer. Studies have shown that serum CXCL3 levels are associated with the progression and poor prognosis of colorectal cancer, and CXCL3 overexpression increases the malignant behavior of tumor cells, while down-regulation of its expression inhibits this phenomenon. The CXCL3 released by macrophages can promote the transformation of fibroblasts into myofibroblasts, thereby promoting the metastasis of pancreatic cancer. However, there are still few studies on CXCL3 in the kidney, and its role in DKD needs to be further explored. In the DKD single cell dataset and the KIT website, we found that CXCL3 was significantly increased in DKD, and was positively correlated with proteinuria and serum creatinine. On the basis of previous bioinformatics analysis and verification, this study further verified that the gene had no DKD damage in DKD and diabetes, the mRNA expression level of peripheral blood PBMC in normal control and the expression level in serum and urine ( Elisa ), and further verified in kidney tissue, animal and cell levels, looking for new biomarkers for DKD.
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120 participants in 3 patient groups
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Data sourced from clinicaltrials.gov
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