There have been over 400 million patients of diabetes mellitus globally, and this number is expected to increase to 600 million by 2035. And 20% of diabetes mellitus patients may develop diabetic nephropathy (DN). To date, the DN is the most common cause of end-stage renal disease, leading to the low life quality and high mortality of DN patients.
Renal tubulointerstitial disease is the major pathogenesis of DN, which is also corelated with deterioration of renal function. However, research has yet to reveal the exact mechanism of tubulointerstitial disease in DN. Furthermore, it remains to be discovered that how renal tubular epithelial cell and macrophage involve in tubulointerstitial disease, thereby to modulate the changing process of renal tubular epithelial cell and macrophage to prevent or reverse diabetic kidney disease.
This Research Topic aims to call for original research and reviews that contribute to the new findings of the molecular basis of the renal tubulointerstitial disease in diabetic nephropathy. Specially we welcome research in renal tubular epithelial cell and macrophage in diabetic nephropathy.
We welcome submissions focusing but not limited to:
• The molecular mechanisms of renal tubular epithelial cell damage leading to tubulointerstitial disease in diabetic nephropathy.
• Ferroptosis of renal tubular epithelial cell and its association with diabetic nephropathy.
• How the macrophage is involved in the process of tubulointerstitial disease in diabetic nephropathy.
• The crosstalk of renal tubular epithelial cell and macrophage in diabetic nephropathy.
• The regulatory role of factors or drugs in the processing of tubulointerstitial fibrosis in diabetic nephropathy.
There have been over 400 million patients of diabetes mellitus globally, and this number is expected to increase to 600 million by 2035. And 20% of diabetes mellitus patients may develop diabetic nephropathy (DN). To date, the DN is the most common cause of end-stage renal disease, leading to the low life quality and high mortality of DN patients.
Renal tubulointerstitial disease is the major pathogenesis of DN, which is also corelated with deterioration of renal function. However, research has yet to reveal the exact mechanism of tubulointerstitial disease in DN. Furthermore, it remains to be discovered that how renal tubular epithelial cell and macrophage involve in tubulointerstitial disease, thereby to modulate the changing process of renal tubular epithelial cell and macrophage to prevent or reverse diabetic kidney disease.
This Research Topic aims to call for original research and reviews that contribute to the new findings of the molecular basis of the renal tubulointerstitial disease in diabetic nephropathy. Specially we welcome research in renal tubular epithelial cell and macrophage in diabetic nephropathy.
We welcome submissions focusing but not limited to:
• The molecular mechanisms of renal tubular epithelial cell damage leading to tubulointerstitial disease in diabetic nephropathy.
• Ferroptosis of renal tubular epithelial cell and its association with diabetic nephropathy.
• How the macrophage is involved in the process of tubulointerstitial disease in diabetic nephropathy.
• The crosstalk of renal tubular epithelial cell and macrophage in diabetic nephropathy.
• The regulatory role of factors or drugs in the processing of tubulointerstitial fibrosis in diabetic nephropathy.
