The Mechanism of Hyperglycemia-Induced Renal Cell Injury in Diabetic Nephropathy Disease: An Update.
Tong WuLei DingVivian AndohJiaxin ZhangLiang ChenPublished in: Life (Basel, Switzerland) (2023)
Diabetic Nephropathy (DN) is a serious complication of type I and II diabetes. It develops from the initial microproteinuria to end-stage renal failure. The main initiator for DN is chronic hyperglycemia. Hyperglycemia (HG) can stimulate the resident and non-resident renal cells to produce humoral mediators and cytokines that can lead to functional and phenotypic changes in renal cells and tissues, interference with cell growth, interacting proteins, advanced glycation end products (AGEs), etc., ultimately resulting in glomerular and tubular damage and the onset of kidney disease. Therefore, poor blood glucose control is a particularly important risk factor for the development of DN. In this paper, the types and mechanisms of DN cell damage are classified and summarized by reviewing the related literature concerning the effect of hyperglycemia on the development of DN. At the cellular level, we summarize the mechanisms and effects of renal damage by hyperglycemia. This is expected to provide therapeutic ideas and inspiration for further studies on the treatment of patients with DN.
Keyphrases
- diabetic nephropathy
- diabetic rats
- oxidative stress
- induced apoptosis
- blood glucose
- cell cycle arrest
- high glucose
- single cell
- type diabetes
- systematic review
- glycemic control
- patient safety
- immune response
- gene expression
- cell therapy
- signaling pathway
- endoplasmic reticulum stress
- stem cells
- quality improvement
- endothelial cells
- blood pressure
- cell death
- mesenchymal stem cells
- insulin resistance
- living cells
- fluorescent probe