血管紧张素转换酶2与糖尿病肾病

The identification of angiotensin-converting enzyme (ACE)2 opened new recognition of renin-angiotensin system (RAS). ACE2 degrades Ang Ⅱ to Ang (1-7), maintains homeostasis of RAS with ACE. Studies have revealed that ACE2 has important functions in diabetic nephropathy. It may be a target for drug and is used as gene therapy for diabetic nephropathy. Amplifying ACE2 activity may have a potential therapeutic role for diabetic nephropathy.     

血管紧张素转换酶2与糖尿病肾病

The identification of angiotensin-converting enzyme (ACE)2 opened new recognition of renin-angiotensin system (RAS). ACE2 degrades Ang Ⅱ to Ang (1-7), maintains homeostasis of RAS with ACE. Studies have revealed that ACE2 has important functions in diabetic nephropathy. It may be a target for drug and is used as gene therapy for diabetic nephropathy. Amplifying ACE2 activity may have a potential therapeutic role for diabetic nephropathy.     

血管紧张素转换酶2与糖尿病肾病

The identification of angiotensin-converting enzyme (ACE)2 opened new recognition of renin-angiotensin system (RAS). ACE2 degrades Ang Ⅱ to Ang (1-7), maintains homeostasis of RAS with ACE. Studies have revealed that ACE2 has important functions in diabetic nephropathy. It may be a target for drug and is used as gene therapy for diabetic nephropathy. Amplifying ACE2 activity may have a potential therapeutic role for diabetic nephropathy.     

血管紧张素转换酶2与糖尿病肾病

The identification of angiotensin-converting enzyme (ACE)2 opened new recognition of renin-angiotensin system (RAS). ACE2 degrades Ang Ⅱ to Ang (1-7), maintains homeostasis of RAS with ACE. Studies have revealed that ACE2 has important functions in diabetic nephropathy. It may be a target for drug and is used as gene therapy for diabetic nephropathy. Amplifying ACE2 activity may have a potential therapeutic role for diabetic nephropathy.     

血管紧张素转换酶2与糖尿病肾病

The identification of angiotensin-converting enzyme (ACE)2 opened new recognition of renin-angiotensin system (RAS). ACE2 degrades Ang Ⅱ to Ang (1-7), maintains homeostasis of RAS with ACE. Studies have revealed that ACE2 has important functions in diabetic nephropathy. It may be a target for drug and is used as gene therapy for diabetic nephropathy. Amplifying ACE2 activity may have a potential therapeutic role for diabetic nephropathy.     

血管紧张素转换酶2与糖尿病肾病

The identification of angiotensin-converting enzyme (ACE)2 opened new recognition of renin-angiotensin system (RAS). ACE2 degrades Ang Ⅱ to Ang (1-7), maintains homeostasis of RAS with ACE. Studies have revealed that ACE2 has important functions in diabetic nephropathy. It may be a target for drug and is used as gene therapy for diabetic nephropathy. Amplifying ACE2 activity may have a potential therapeutic role for diabetic nephropathy.     

血管紧张素转换酶2研究新进展

血管紧张素转换酶(ACE)是一种锌指金属蛋白酶,对肾素-血管紧张素系统(RAS)有关键调控作用.ACE 2主要分布在心脏、肾脏和睾丸,能水解血管紧张素(Ang)Ⅰ,产生Ang 1-9,还能水解RAS中的主要物质AngⅡ,产生具有血管扩张作用的Ang 1-7.研究表明ACE 2可能在RAS中扮演与ACE相反的角色,达到血管收缩和舒张之间的平衡,与高血压、心力衰竭及糖尿病肾病等关系密切.     

血管紧张素转换酶2研究进展

血管紧张素转换酶(ACE)是一种锌指金属蛋白酶,对肾素—血管紧张素系统(RAS)有关键调控作用。ACE2是最近在啮齿类动物和人类中发现的一种ACE相关的羧基肽酶,主要分布在心脏、肾脏和睾丸。ACE2能水解血管紧张素(Ang)Ⅰ,产生Ang-(1-9),还能水解RAS中的主要物质AngⅡ,产生具有血管扩张作用的Ang-(1-7)。很多研究表明,ACE2可能在RAS中扮演与ACE相反的角色,以达到血管收缩和舒张的平衡,并与高血压的发生关系密切。ACE2基因敲除小鼠的心功能受到损害。糖尿病肾病小鼠肾小管的ACE2水平明显下降,提高ACE2水平则可能预防糖尿病肾病的发生和进展。但ACE2的具体作用机制还需进一步研究。     

血管紧张素转换酶2与糖尿病

肾素-血管紧张素系统（RAS）的过度激活在糖尿病及其慢性并发症的发生发展中发挥重要作用。血管紧张素转换酶（ACE）2作为RAS的新成员,可高效水解血管紧张素（Ang）Ⅱ生成Ang（1-7）,并竞争性作用于ACE的底物AngⅠ,与ACE共同调节RAS稳态。ACE2可改善胰岛血供、胰岛素分泌、减少胰岛纤维化及胰岛素抵抗,并延缓糖尿病慢性并发症的发生发展。深入研究ACE2,对防治糖尿病及其慢性并发症具有重要意义。     

高糖对肾小管上皮细胞ACE/ACE2表达的影响

体外培养的HK-2细胞分为正常对照组(NG组)、高糖组(HG组)、渗透压对照组(MG组),检测细胞ACE、ACE2 mRNA和蛋白表达及细胞上清液血管紧张素Ⅱ的浓度.结果 在NG组,正常培养的HK-2细胞即存在ACE、ACE2 mRNA及蛋白表达.在HG组HK-2细胞,ACE mRNA及蛋白表达较NG组升高,而ACE2mRNA及蛋白表达降低.在HG组血管紧张素Ⅱ水平较NG组显著升高.结果 表明高糖可促进体外培养的HK-2细胞ACE表达、抑制ACE2表达,进而促进血管紧张素Ⅱ合成.

Abstract：

HK-2 cells cultured in vitro were divided into three groups: normal glucose group ( NG ), high glucose group( HG), and mannitol group(MG). The expression of angiotensin-converting enzyme( ACE ) and ACE2 mRNA in HK-2 cells was detected. The concentration of angiotensin Ⅱ ( Ang Ⅱ ) in the culture medium was detected. The mRNA and protein expression of ACE and ACE2 existed in normal cultured HK-2 ( NG group ). In comparison with NG group, the mRNA and protein expressions of ACE in HG group increased significantly ( P＜0. 01 ), and the expression of ACE2 mRNA decreased significantly( P＜0. 01 ). The level of Ang Ⅱ in HG group was significantly higher than in NG group( P＜0. 05 ). The result show that high glucose may induce ACE expression and inhibit ACE2 expression, then promote synthesis of Ang Ⅱ in proximal tubular cells.