AI Article Synopsis
- This study investigates the role of FNDC5 in the development of atherosclerosis using a mouse model fed a high-fat diet.
- After analyzing various cholesterol levels and aortic plaque metrics, it was found that FNDC5 overexpression improved metabolic parameters in high-fat diet mice.
- The results suggest that FNDC5 may slow down atherosclerosis by activating a specific signaling pathway (PPARα/HO-1).
Article Abstract
Introduction: This study attempted to observe the role of fibronectin type III domain-containing protein 5 (FNDC5) in atherosclerosis development and the underlying mechanism.
Methods: After being fed a high-fat diet (HFD), ApoE-/- mice were injected with saline, control adenovirus (Ad-vector), or FNDC5 overexpressing adenovirus (Ad-FNDC5). ApoE-/- mice fed with a chow diet were considered the control. After 12 weeks of treatment, the levels of serum high-density lipoprotein cholesterol (HDL-C), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), triglyceride (TG), and irisin were detected by commercial kits.
Results: Compared with the control, the serum TG, TC, and LDL-C levels, aortic plaque area, and weight were significantly increased, while serum HDL-C and irisin levels were reduced in HFD mice. Treating with Ad-FNDC5 could alleviate these changes in HFD mice and cause the activation of PPARα/HO-1 signaling in aortic tissue. After co-treating with GW6471, a PPARα antagonist, the effects of Ad-FNDC5 on the weight, serum LDL-C, TC, TG, and HDL-C levels, and aortic plaque of HFD mice were partly blocked.
Conclusion: Elevated FNDC5 has a delaying effect on atherosclerotic plaque formation, which may be related to the upregulation of PPARα/HO-1 signaling.
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| http://dx.doi.org/10.1159/000531585 | DOI Listing |
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