Fibroblast growth factor 21 deletion aggravates diabetes-induced pathogenic changes in the aorta in type 1 diabetic miceReport as inadecuate




Fibroblast growth factor 21 deletion aggravates diabetes-induced pathogenic changes in the aorta in type 1 diabetic mice - Download this document for free, or read online. Document in PDF available to download.

Cardiovascular Diabetology

, 14:77

First Online: 11 June 2015Received: 15 January 2015Accepted: 02 June 2015

Abstract

Fibroblast growth factor 21 FGF21 is an important regulator in glucose and lipid metabolism, and has been considered as a potential therapy for diabetes. The effect of FGF21 on the development and progression of diabetes-induced pathogenic changes in the aorta has not currently been addressed. To characterize these effects, type 1 diabetes was induced in both FGF21 knockout FGF21KO and C57BL-6 J wild type WT mice via multiple-dose streptozotocin injection. FGF21KO diabetic mice showed both earlier and more severe aortic remodeling indicated by aortic thickening, collagen accumulation and fibrotic mediator connective tissue growth factor expression. This was accompanied by significant aortic cell apoptosis than in WT diabetic mice. Further investigation found that FGF21 deletion exacerbated aortic inflammation and oxidative stress reflected by elevated expression of tumor necrosis factor α and transforming growth factor β, and the accumulation of 3-nitrotyrocine and 4-Hydroxynonenal. FGF21 administration can reverse the pathologic changes in FGF21KO diabetic mice. These findings demonstrate that FGF21 deletion aggravates aortic remodeling and cell death probably via exacerbation of aortic inflammation and oxidative stress. This marks FGF21 as a potential therapy for the treatment of aortic damage due to diabetes.

KeywordsFibroblast growth factor 21 Vascular damage Diabetes Oxidative stress  Download fulltext PDF



Author: Xiaoqing Yan - Jun Chen - Chi Zhang - Jun Zeng - Shanshan Zhou - Zhiguo Zhang - Xuemian Lu - Jing Chen - Wenke Feng - Xia

Source: https://link.springer.com/article/10.1186/s12933-015-0241-0







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