Implications of treatment that target protective mechanisms against diabetic nephropathy.
Diabetes results in vascular changes and dysfunction, and vascular complications are the leading cause of morbidity and mortality in diabetic patients. There has been a continual increase in the number of diabetic nephropathy patients and epidemic increases in the number of patients progressing to end-stage renal diseases. To identify targets for therapeutic intervention, most studies have focused on understanding how abnormal levels of glucose metabolites cause diabetic nephropathy, which is of paramount importance in devising strategies to combat the development and progression of diabetic nephropathy. However, less studied than the systemic toxic mechanisms, hyperglycemia and dyslipidemia might inhibit the endogenous vascular protective factors such as insulin, vascular endothelial growth factor, and platelet-derived growth factor. In this review, we highlight the importance of enhancing endogenous protective factors to prevent or delay diabetic nephropathy.
Research Division, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA.
Akira
A
Mima
Weier
W
Qi
George L
GL
King
D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D000975:Antioxidants / Q000627:therapeutic use; D003928:Diabetic Nephropathies / Q000209:etiology / Q000378:metabolism* / Q000517:prevention & control*; D050171:Dyslipidemias / Q000150:complications / Q000378:metabolism*; D017127:Glycation End Products, Advanced / Q000037:antagonists & inhibitors / Q000378:metabolism; D006801:Humans; D006943:Hyperglycemia / Q000150:complications / Q000378:metabolism*; D007328:Insulin / Q000378:metabolism; D010982:Platelet-Derived Growth Factor / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D017127:Glycation End Products, Advanced; D007328:Insulin; D010982:Platelet-Derived Growth Factor; D042461:Vascular Endothelial Growth Factor A