دورية أكاديمية
Kinin B1 Receptor Antagonism Prevents Acute Kidney Injury to Chronic Kidney Disease Transition in Renal Ischemia-Reperfusion by Increasing the M2 Macrophages Population in C57BL6J Mice
| العنوان: | Kinin B1 Receptor Antagonism Prevents Acute Kidney Injury to Chronic Kidney Disease Transition in Renal Ischemia-Reperfusion by Increasing the M2 Macrophages Population in C57BL6J Mice |
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| المؤلفون: | Gabriel Rufino Estrela, Raisa Brito Santos, Alexandre Budu, Adriano Cleis de Arruda, Jonatan Barrera-Chimal, Ronaldo Carvalho Araújo |
| المصدر: | Biomedicines, Vol 11, Iss 8, p 2194 (2023) |
| بيانات النشر: | MDPI AG, 2023. |
| سنة النشر: | 2023 |
| المجموعة: | LCC:Biology (General) |
| مصطلحات موضوعية: | chronic kidney disease, acute kidney disease, kinins, inflammation, experimental disease model, Biology (General), QH301-705.5 |
| الوصف: | Background: Chronic kidney disease (CKD) is a multifactorial, world public health problem that often develops as a consequence of acute kidney injury (AKI) and inflammation. Strategies are constantly sought to avoid and mitigate the irreversibility of this disease. One of these strategies is to decrease the inflammation features of AKI and, consequently, the transition to CKD. Methods: C57Bl6J mice were anesthetized, and surgery was performed to induce unilateral ischemia/reperfusion as a model of AKI to CKD transition. For acute studies, the animals received the Kinin B1 receptor (B1R) antagonist before the surgery, and for the chronic model, the animals received one additional dose after the surgery. In addition, B1R genetically deficient mice were also challenged with ischemia/reperfusion. Results: The absence and antagonism of B1R improved the kidney function following AKI and prevented CKD transition, as evidenced by the preserved renal function and prevention of fibrosis. The protective effect of B1R antagonism or deficiency was associated with increased levels of macrophage type 2 markers in the kidney. Conclusions: The B1R is pivotal to the evolution of AKI to CKD, and its antagonism shows potential as a therapeutic tool in the prevention of CKD following AKI. |
| نوع الوثيقة: | article |
| وصف الملف: | electronic resource |
| اللغة: | English |
| تدمد: | 11082194 2227-9059 |
| Relation: | https://www.mdpi.com/2227-9059/11/8/2194; https://doaj.org/toc/2227-9059 |
| DOI: | 10.3390/biomedicines11082194 |
| URL الوصول: | https://doaj.org/article/a78e2a2826e24ff2bd86642872f54fe0 |
| رقم الأكسشن: | edsdoj.78e2a2826e24ff2bd86642872f54fe0 |
| قاعدة البيانات: | Directory of Open Access Journals |
Full Text Finder | تدمد: | 11082194 22279059 |
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| DOI: | 10.3390/biomedicines11082194 |