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Fibroblast growth factor 21 deletion aggravates diabetes-induced pathogenic changes in the aorta in type 1 diabetic
Xiaoqing Yan1,2,3,4, Jun Chen1,4,5, Chi Zhang1,3
1Chinese-American Research Institute for Diabetic Complications at the Wenzhou Medical University, Wenzhou, China.
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.
Insights
Fibroblast growth factor 21 (FGF21) deficiency worsens aortic remodeling and cell death in diabetic mice by increasing inflammation and oxidative stress. FGF21 administration can reverse these damaging effects, suggesting its therapeutic potential for diabetic aortic complications.
Area of Science:
- Endocrinology
- Cardiovascular Biology
- Metabolic Diseases
Background:
- Fibroblast growth factor 21 (FGF21) regulates glucose and lipid metabolism, showing therapeutic promise for diabetes.
- The impact of FGF21 on diabetes-associated aortic pathology remains uncharacterized.
Purpose of the Study:
- To investigate the role of FGF21 in diabetes-induced aortic remodeling and cellular changes.
- To determine if FGF21 administration can ameliorate these pathological alterations.
Main Methods:
- Type 1 diabetes was induced in FGF21 knockout (FGF21KO) and wild-type (WT) mice using streptozotocin.
- Aortic remodeling, cell apoptosis, inflammation, and oxidative stress markers were assessed.
- FGF21 was administered to FGF21KO diabetic mice to evaluate therapeutic effects.
Main Results:
- FGF21KO diabetic mice exhibited accelerated and more severe aortic thickening, collagen accumulation, and fibrosis.
- Increased aortic cell apoptosis, inflammation (TNF-α, TGF-β), and oxidative stress (3-nitrotyrosine, 4-HNE) were observed in FGF21KO diabetic mice.
- FGF21 treatment reversed the pathological aortic changes in FGF21KO diabetic mice.
Conclusions:
- FGF21 deficiency exacerbates aortic remodeling and cell death in diabetes, likely through increased inflammation and oxidative stress.
- FGF21 plays a protective role against diabetes-induced aortic damage.
- FGF21 represents a potential therapeutic target for treating aortic complications in diabetes.
