Academic Journal

Decreased TRPM7 alleviates high glucose-induced renal tubular epithelial cell injury by inhibiting the HMGB1/TLR4 signaling pathway

التفاصيل البيبلوغرافية
العنوان: Decreased TRPM7 alleviates high glucose-induced renal tubular epithelial cell injury by inhibiting the HMGB1/TLR4 signaling pathway
المؤلفون: Wei Feng, Zheng-Yong Cao, Fu-Min Guan, Hong Chen
المصدر: Asian Pacific Journal of Tropical Biomedicine, Vol 13, Iss 9, Pp 393-402 (2023)
بيانات النشر: Wolters Kluwer Medknow Publications, 2023.
سنة النشر: 2023
المجموعة: LCC:Arctic medicine. Tropical medicine
LCC:Biology (General)
مصطلحات موضوعية: diabetic nephropathy, trpm7, hmgb1/tlr4, high glucose, renal tubular epithelial cell, Arctic medicine. Tropical medicine, RC955-962, Biology (General), QH301-705.5
الوصف: 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.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 2221-1691
2588-9222
Relation: http://www.apjtb.org/article.asp?issn=2221-1691;year=2023;volume=13;issue=9;spage=393;epage=402;aulast=Feng; https://doaj.org/toc/2221-1691; https://doaj.org/toc/2588-9222
DOI: 10.4103/2221-1691.385570
URL الوصول: https://doaj.org/article/573029f0c1e94e05a6b336dab7f1c5e3
رقم الانضمام: edsdoj.573029f0c1e94e05a6b336dab7f1c5e3
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:22211691
25889222
DOI:10.4103/2221-1691.385570