摘要
血管紧张素Ⅱ1型受体(AT1R)介导的免疫反应及相关内质网应激(ERS)反应所致肾脏细胞凋亡在DN进展中作用明显。阐述CKD进程中AT1R及相关ERS反应有助于在受体和分子水平完善其发病机制,有可能为延缓甚至逆转CKD进展、防止其转变为终末期肾病提供新的治疗靶点。
Recent advances shed light on the mechanisms of kidney cell apoptosis which is attributed to endoplasmic reticulum stress (ERS) and immune response mediated by angiotensin Ⅱ type 1 receptor (AT1R).To enrich the cellular and molecular mechanisms of DN,the further study of AT1 R and its autoantibody,as well as the relative ERS response is very necessary.
出处
《中国糖尿病杂志》
CAS
CSCD
北大核心
2014年第8期759-761,共3页
Chinese Journal of Diabetes
基金
湖北省自然科学基金(2011CHC001)
关键词
糖尿病肾病
血管紧张素Ⅱ1型受体
内质网应激
Diabetic nephropathy(DN)
Angiotensin Ⅱ type 1 receptor (AT1 R)
Endoplasmic reticulum stress (ERS)