The following is the summary of “Uncover diagnostic immunity/hypoxia/ferroptosis/epithelial mesenchymal transformation-related CCR5, CD86, CD8A, ITGAM, and PTPRC in kidney transplantation patients with allograft rejection” published in the November 2022 issue of Renal failure by He, et al.
The purpose of this research was to find predictive biomarkers, pathways, and novel medications associated with immunity, hypoxia, ferroptosis, and epithelial mesenchymal transition (EMT) in allograft rejection in kidney transplant patients. First, data on gene expression were downloaded, then the differentially expressed genes (DEGs), weighted gene co-expression network analysis (WGCNA), and protein–protein interaction (PPI) analysis were performed in order.
The second step was the building of a diagnostic model based on the key genes, which was then followed by an examination of the link between immune/hypoxia/ferroptosis/EMT and the key diagnostic genes. In the end, medication prediction was performed using diagnostic key genes. Further research led to the identification of 5 diagnostic genes, including CCR5, CD86, CD8A, ITGAM, and PTPRC. All of these genes had a positive correlation with allograft rejection following the kidney transplant. About 5 diagnostic genes showed a substantial positive correlation with highly infiltrating immune cells, highly expressed hypoxia-related genes, and an activated status of EMT.
Ferroptosis has a complicated regulatory interaction with the five diagnostic genes, as shown by suppressors of ferroptosis (SOFs) and drivers of ferroptosis (DOFs). ABATACEPT, MARAVIROC, and CLARITHROMYCIN all had CD86, CCR5, and ITGAM as their primary pharmacological targets, respectively. Both PREDNISONE and EPOETIN BETA had PTPRC as their intended pharmacological target. In conclusion, the study has the potential to be helpful in understanding changes in the microenvironment that occur after transplantation, which may encourage or sustain the development of allograft rejection following kidney transplantation.
Source: tandfonline.com/doi/full/10.1080/0886022X.2022.2141648
