One-third of both type 1 diabetes and type 2 diabetes patients suffer from diabetic kidney disease (DKD), which is the leading cause of new-onset end-stage renal disease (ESRD), and is also associated with cardiovascular disease and high public health care costs. Although the development of clinical therapy for DKD has made great progress, the progression of DKD still cannot be controlled. Therefore, further study of the pathogenesis of DKD and improvements in DKD treatment are crucial for prognosis. Increasing evidence suggests that there is cross talk between cells such as between glomerular endothelial cells (GEC) and mesangial cells, GEC and podocytes, GEC and tubular epithelial cells, and immunocytes and kidney cells. Therefore, more research on the cell crosstalk in the pathogenesis of DKD could provide mechanistic clues that underlie DKD and provide novel avenues for therapeutic intervention.
This Research Topic focuses on cell crosstalk in DKD, including glomerular cells, tubular cells and resident or infiltrated immunocytes, with a particular interest on signal communications, redox, cellular targets that mediate proteinuria, glomerular sclerosis and interstitial fibrosis of DKD. We welcome submissions of Original Research and Reviews on the subtopics below, with function validation of in vitro or in vivo methods:
? Glomerular endothelial cell cross talk with podocytes in DKD
? Novel cell types identified by single cell RNA-seq in the development of DKD
? Immunocyte crosstalk with tubular epithelial cell or mesangial cells in the inflammation, interstitial fibrosis or glomerular sclerosis of DKD
? Crosstalk between tubular epithelial cells and glomerular endothelial cells in DKD
One-third of both type 1 diabetes and type 2 diabetes patients suffer from diabetic kidney disease (DKD), which is the leading cause of new-onset end-stage renal disease (ESRD), and is also associated with cardiovascular disease and high public health care costs. Although the development of clinical therapy for DKD has made great progress, the progression of DKD still cannot be controlled. Therefore, further study of the pathogenesis of DKD and improvements in DKD treatment are crucial for prognosis. Increasing evidence suggests that there is cross talk between cells such as between glomerular endothelial cells (GEC) and mesangial cells, GEC and podocytes, GEC and tubular epithelial cells, and immunocytes and kidney cells. Therefore, more research on the cell crosstalk in the pathogenesis of DKD could provide mechanistic clues that underlie DKD and provide novel avenues for therapeutic intervention.
This Research Topic focuses on cell crosstalk in DKD, including glomerular cells, tubular cells and resident or infiltrated immunocytes, with a particular interest on signal communications, redox, cellular targets that mediate proteinuria, glomerular sclerosis and interstitial fibrosis of DKD. We welcome submissions of Original Research and Reviews on the subtopics below, with function validation of in vitro or in vivo methods:
? Glomerular endothelial cell cross talk with podocytes in DKD
? Novel cell types identified by single cell RNA-seq in the development of DKD
? Immunocyte crosstalk with tubular epithelial cell or mesangial cells in the inflammation, interstitial fibrosis or glomerular sclerosis of DKD
? Crosstalk between tubular epithelial cells and glomerular endothelial cells in DKD
