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肾小管特异性血管紧张素原缺失可减弱1型糖尿病小鼠模型中SGLT2的表达并改善糖尿病肾病。

Renal Tubule-Specific Angiotensinogen Deletion Attenuates SGLT2 Expression and Ameliorates Diabetic Kidney Disease in Murine Models of Type 1 Diabetes.

作者信息

Yang Wen-Xia, Su Ke, Liao Min-Chun, Zhou Jing, Peng Junzheng, Hébert Marie-Josée, Leal Daniel N, Yamashita Michifumi, Miyata Kana N, Filep Janos G, Ingelfinger Julie R, Zhang Shao-Ling, Chan John S D

机构信息

Centre de Recherche, Centre Hospitalier de l'Université de Montréal (CRCHUM) and Département de Médecine, Université de Montréal, Montréal, Quebec, Canada.

Department of Pathology and Laboratory Medicine, Cedars-Sinai Medical Center, Los Angeles, CA.

出版信息

Diabetes. 2025 Apr 1;74(4):554-568. doi: 10.2337/db24-0553.

DOI:10.2337/db24-0553
PMID:39752561
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11926280/
Abstract

Renin-angiotensin system (RAS) activation plays an important role in the progression of diabetic kidney disease (DKD). However, systemic RAS blockade alone is insufficient to reverse DKD progression. We hypothesized that intrarenal renin-angiotensin system (iRAS) activation plays a crucial role in the progression of DKD. We sought to elucidate the role of the iRAS in DKD progression. Selective deletion of angiotensinogen in renal tubules ameliorated the pathological features of DKD. Our study indicates that iRAS inactivation may be a potential approach for preventing DKD disease severity and its progression.

摘要

肾素-血管紧张素系统(RAS)激活在糖尿病肾病(DKD)进展中起重要作用。然而,仅全身性RAS阻断不足以逆转DKD进展。我们推测肾内肾素-血管紧张素系统(iRAS)激活在DKD进展中起关键作用。我们试图阐明iRAS在DKD进展中的作用。肾小管中血管紧张素原的选择性缺失改善了DKD的病理特征。我们的研究表明,iRAS失活可能是预防DKD疾病严重程度及其进展的一种潜在方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62a9/11926280/61f4ede016a6/db240553f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62a9/11926280/7aeb442186c4/db240553fGA.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62a9/11926280/ca78b9747a42/db240553f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62a9/11926280/0c49ad2f0fdf/db240553f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62a9/11926280/1a52763a00ad/db240553f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62a9/11926280/728e23668f42/db240553f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62a9/11926280/5eb0e292e3b7/db240553f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62a9/11926280/61f4ede016a6/db240553f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62a9/11926280/7aeb442186c4/db240553fGA.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62a9/11926280/d587fcbf4d64/db240553f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62a9/11926280/dc53ad7cd0e9/db240553f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62a9/11926280/ca78b9747a42/db240553f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62a9/11926280/0c49ad2f0fdf/db240553f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62a9/11926280/1a52763a00ad/db240553f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62a9/11926280/728e23668f42/db240553f6.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62a9/11926280/61f4ede016a6/db240553f8.jpg

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本文引用的文献

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Antioxidants (Basel). 2023 Sep 4;12(9):1715. doi: 10.3390/antiox12091715.
2
Renal insulin resistance in type 2 diabetes mellitus and progression of chronic kidney disease: potential pathogenic mechanisms.2型糖尿病中的肾胰岛素抵抗与慢性肾脏病的进展:潜在的致病机制
Expert Rev Endocrinol Metab. 2022 Nov;17(6):523-532. doi: 10.1080/17446651.2022.2131534. Epub 2022 Oct 6.
3
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