Role of cofilin in kidney disease / 中南大学学报(医学版)

Cofilin is a actin-binding protein in eukaryotic cells. It plays a role in maintaining the steady state of the internal environment through regulating actin dynamics, which contributes to the development of various kinds of diseases. In recent 20 years, cofilin has been widely attracted due to its regulatory effect on cell phenotype, gene transcription, apoptosis and inflammation in renal tissue. Cofilin plays a regulatory role in pathological changes in proteinuria diseases such as minimal change nephropathy, focal segmental glomerulosclerosis, membranous nephropathy, and IgA nephropathy. It could be one of the diagnosis index for glomerular podocyte injury. At the same time, cofilin plays a key role in maintaining the polarity and function of proximal tubular epithelial cells and it is involved in the regulation of kidney inflammation in a variety of kidney diseases, such as renal ischemia/reperfusion injury, diabetic nephropathy, and hypertensive nephropathy reaction. In addition, cofilin plays an important role in epithelial-to-mesenchymal transition (EMT) of tumor cells and epithelial cells in various tissues, suggesting that cofilin may be involved in the regulation of peritoneal dialysis-related EMT and fibrosis. Cofilin might turn into the new diagnosis and treatment target of kidney diseases.

Advances in molecular genetics research of IgA nephropathy / 中南大学学报(医学版)

Immunoglobulin A nephropathy (IgAN), which can develop into end-stage renal disease, is the most common primary glomerulonephritis. The pathogenesis of IgAN is not clear. Many studies have confirmed that genetic susceptibility is associated with IgAN, and it belongs to polygenic disease. Some studies have found that IgAN is associated with chromosome 6q22-23, 2q36 by linkage analysis, and several candidate genes have been confirmed to be associated with IgAN, such as angiotensin converting enzyme, Fc fragment of IgA receptor, human leukocyte antigen. In recent years, as the progression of molecular genetics and the Human Genome Project, more attention has been paid to the role of genetic factors in the pathogenesis of IgAN.