去纤维蛋白原能以一种与 CX3CR1 无关的方式改善视网膜小胶质细胞增多和炎症。

IF 3.9 4区医学 Q2 NEUROSCIENCES

ASN NEURO Pub Date : 2022-01-01 DOI:10.1177/17590914221131446

Borna Sarker, Sandra M Cardona, Kaira A Church, Difernando Vanegas, Priscila Velazquez, Colin Rorex, Derek Rodriguez, Andrew S Mendiola, Timothy S Kern, Nadia D Domingo, Robin Stephens, Isabel A Muzzio, Astrid E Cardona

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引用次数: 0

摘要

摘要说明：糖尿病人和小鼠视网膜显示出明显的小胶质细胞形态激活和与炎症相关的血管异常。在糖尿病小鼠视网膜中，使用 ancrod 进行药理纤维蛋白原耗竭可抑制小胶质细胞形态改变，解决纤维蛋白原积聚问题，挽救轴突完整性并减轻炎症。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

Defibrinogenation Ameliorates Retinal Microgliosis and Inflammation in A CX3CR1-Independent Manner.

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Defibrinogenation Ameliorates Retinal Microgliosis and Inflammation in A CX3CR1-Independent Manner.

Summary statement: Diabetic human and murine retinas revealed pronounced microglial morphological activation and vascular abnormalities associated with inflammation. Pharmacological fibrinogen depletion using ancrod dampened microglial morphology alterations, resolved fibrinogen accumulation, rescued axonal integrity, and reduced inflammation in the diabetic murine retina.

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来源期刊

ASN NEURO NEUROSCIENCES-

CiteScore

7.70

自引率

4.30%

发文量

审稿时长

>12 weeks

期刊介绍： ASN NEURO is an open access, peer-reviewed journal uniquely positioned to provide investigators with the most recent advances across the breadth of the cellular and molecular neurosciences. The official journal of the American Society for Neurochemistry, ASN NEURO is dedicated to the promotion, support, and facilitation of communication among cellular and molecular neuroscientists of all specializations.