Soetikno Vivian, Arozal Wawaimuli, Louisa Melva, Setiabudy Rianto
Department of Pharmacology and Therapeutic, Faculty of Medicine, University of Indonesia, Salemba Raya 6, Jakarta 10430, Indonesia.
Int J Endocrinol. 2014;2014:968681. doi: 10.1155/2014/968681. Epub 2014 Feb 4.
Diabetic nephropathy (DN) lowered quality of life and shortened life expectancy amongst those affected. Evidence indicates interaction between advanced glycation end products (AGEs), activated protein kinase C (PKC) and angiotensin II exacerbate the progression of DN. Inhibitors of angiotensin-converting enzyme (ACEIs), renin angiotensin aldosterone system (RAAS), AGEs, and PKC have been tested for slowing down the progression of DN. The exact molecular drug targets that lead to the amelioration of renal injury in DN are not well understood. This review summarizes the potential therapeutic targets, based on putative mechanism in the progression of the disease.
糖尿病肾病(DN)会降低患者的生活质量并缩短预期寿命。有证据表明,晚期糖基化终末产物(AGEs)、活化蛋白激酶C(PKC)和血管紧张素II之间的相互作用会加剧DN的进展。血管紧张素转换酶抑制剂(ACEIs)、肾素血管紧张素醛固酮系统(RAAS)、AGEs和PKC的抑制剂已被用于测试减缓DN的进展。导致DN肾损伤改善的确切分子药物靶点尚不清楚。本综述基于该疾病进展中的假定机制总结了潜在的治疗靶点。