TRPM7(transient receptor potential cation channel subfamily M member 7)是一种具有离子通道与蛋白激酶活性的双功能膜蛋白,在组织中广泛表达,参与多种细胞功能。近年来,大量研究表明TRPM7不仅在生理过程中发挥重要作用,而且在各种...TRPM7(transient receptor potential cation channel subfamily M member 7)是一种具有离子通道与蛋白激酶活性的双功能膜蛋白,在组织中广泛表达,参与多种细胞功能。近年来,大量研究表明TRPM7不仅在生理过程中发挥重要作用,而且在各种心脏疾病的发生和发展过程中起着关键性作用。因此,本综述分析了TRPM7在多种心脏疾病中(包括心肌纤维化,缺血性心肌病和糖尿病性心肌病)的作用,以了解其在疾病病理生理和发病机制中的潜在作用。展开更多
Objective:To explore the regulatory mechanism of transient receptor potential melastatin-7(TRPM7)in high glucose-induced renal tubular epithelial cell injury.Methods:The expression of TRPM7 in the serum of diabetic ne...Objective:To explore the regulatory mechanism of transient receptor potential melastatin-7(TRPM7)in high glucose-induced renal tubular epithelial cell injury.Methods:The expression of TRPM7 in the serum of diabetic nephropathy patients and high glucose-induced HK-2 cells was detected by RT-qPCR.Then,the TRPM7 interference vector was constructed,and the downstream high mobility group box 1(HMGB1)/Toll-like receptor 4(TLR4)signaling pathway proteins were detected.Next,in addition to interference with TRPM7 expression,overexpression of HMGB1 in high glucose-induced HK-2 cells was performed.Cell activity,apoptosis,oxidative stress levels,and inflammation levels were determined by CCK8,TUNEL,Western blotting,immunofluorescence and related kits.Results:TRPM7 expression was upregulated in the serum of diabetic nephropathy patients and high glucose-induced HK-2 cells.Interference with TRPM7 reduced cell damage,epithelial-mesenchymal transition,oxidative stress,and inflammatory response in high glucose-induced HK-2 cells via inhibiting the HMGB1/TLR4 signaling pathway.However,the effects induced by TRPM7 silencing were abrogated by HMGB1 overexpression.Conclusions:Decreased TRPM7 alleviates high glucose-induced renal tubular epithelial cell injury by inhibiting the HMGB1/TLR4 signaling pathway.Further animal experiments and clinical trials are warranted to verify its effect.展开更多
文摘TRPM7(transient receptor potential cation channel subfamily M member 7)是一种具有离子通道与蛋白激酶活性的双功能膜蛋白,在组织中广泛表达,参与多种细胞功能。近年来,大量研究表明TRPM7不仅在生理过程中发挥重要作用,而且在各种心脏疾病的发生和发展过程中起着关键性作用。因此,本综述分析了TRPM7在多种心脏疾病中(包括心肌纤维化,缺血性心肌病和糖尿病性心肌病)的作用,以了解其在疾病病理生理和发病机制中的潜在作用。
文摘Objective:To explore the regulatory mechanism of transient receptor potential melastatin-7(TRPM7)in high glucose-induced renal tubular epithelial cell injury.Methods:The expression of TRPM7 in the serum of diabetic nephropathy patients and high glucose-induced HK-2 cells was detected by RT-qPCR.Then,the TRPM7 interference vector was constructed,and the downstream high mobility group box 1(HMGB1)/Toll-like receptor 4(TLR4)signaling pathway proteins were detected.Next,in addition to interference with TRPM7 expression,overexpression of HMGB1 in high glucose-induced HK-2 cells was performed.Cell activity,apoptosis,oxidative stress levels,and inflammation levels were determined by CCK8,TUNEL,Western blotting,immunofluorescence and related kits.Results:TRPM7 expression was upregulated in the serum of diabetic nephropathy patients and high glucose-induced HK-2 cells.Interference with TRPM7 reduced cell damage,epithelial-mesenchymal transition,oxidative stress,and inflammatory response in high glucose-induced HK-2 cells via inhibiting the HMGB1/TLR4 signaling pathway.However,the effects induced by TRPM7 silencing were abrogated by HMGB1 overexpression.Conclusions:Decreased TRPM7 alleviates high glucose-induced renal tubular epithelial cell injury by inhibiting the HMGB1/TLR4 signaling pathway.Further animal experiments and clinical trials are warranted to verify its effect.