دورية أكاديمية

Macrophages promote Fibrinogenesis during kidney injury

التفاصيل البيبلوغرافية
العنوان: Macrophages promote Fibrinogenesis during kidney injury
المؤلفون: Hanna Oh, Ohbin Kwon, Min Jung Kong, Kwon Moo Park, Jea-Hyun Baek
المصدر: Frontiers in Medicine, Vol 10 (2023)
بيانات النشر: Frontiers Media S.A., 2023.
سنة النشر: 2023
المجموعة: LCC:Medicine (General)
مصطلحات موضوعية: kidney fibrosis, chronic kidney disease, macrophages, coagulation factor, fibrinogenesis, Medicine (General), R5-920
الوصف: Macrophages (Mø) are widely considered fundamental in the development of kidney fibrosis since Mø accumulation commonly aggravates kidney fibrosis, while Mø depletion mitigates it. Although many studies have aimed to elucidate Mø-dependent mechanisms linked to kidney fibrosis and have suggested various mechanisms, the proposed roles have been mostly passive, indirect, and non-unique to Mø. Therefore, the molecular mechanism of how Mø directly promote kidney fibrosis is not fully understood. Recent evidence suggests that Mø produce coagulation factors under diverse pathologic conditions. Notably, coagulation factors mediate fibrinogenesis and contribute to fibrosis. Thus, we hypothesized that kidney Mø express coagulation factors that contribute to the provisional matrix formation during acute kidney injury (AKI). To test our hypothesis, we probed for Mø-derived coagulation factors after kidney injury and uncovered that both infiltrating and kidney-resident Mø produce non-redundant coagulation factors in AKI and chronic kidney disease (CKD). We also identified F13a1, which catalyzes the final step of the coagulation cascade, as the most strongly upregulated coagulation factor in murine and human kidney Mø during AKI and CKD. Our in vitro experiments revealed that the upregulation of coagulation factors in Mø occurs in a Ca2 + −dependent manner. Taken together, our study demonstrates that kidney Mø populations express key coagulation factors following local injury, suggesting a novel effector mechanism of Mø contributing to kidney fibrosis.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 2296-858X
73849332
Relation: https://www.frontiersin.org/articles/10.3389/fmed.2023.1206362/full; https://doaj.org/toc/2296-858X
DOI: 10.3389/fmed.2023.1206362
URL الوصول: https://doaj.org/article/2ff72db753c04a73849332f1db2970aa
رقم الأكسشن: edsdoj.2ff72db753c04a73849332f1db2970aa
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:2296858X
73849332
DOI:10.3389/fmed.2023.1206362