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Updated: May 26, 2026

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
Published on: June 3, 2018
Fibroblast growth factor 21 as a possible endogenous factor inhibits apoptosis in cardiac endothelial cells
Yun Lü1, Jing-Hua Liu, Li-Ke Zhang
1Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, Beijing 100029, China.
Background:
Fibroblast growth factor 21 (FGF21) is a new member of FGF super family that is an important endogenous regulator for systemic glucose and lipid metabolism. This study aimed to explore whether FGF21 reduces atherosclerotic injury and prevents endothelial dysfunction as an independent protection factor.
Methods:
The present study was designed to investigate the changes of FGF21 levels induced by oxidized-low density lipoprotein (ox-LDL), and the changes of apoptosis affected by regulating FGF21 expression. The FGF21 mRNA levels of cultured cardiac microvascular endothelial cells (CMECs) were determined by real time-PCR and the protein concentration in culture media was detected by enzyme-linked immunosorbent assay. We analyzed the different expression levels of untreated controls and CMECs incubated with ox-LDL, and the changes of CMECs apoptosis initiated by the enhancement or suppression of FGF21 levels.
Results:
The secretion levels of FGF21 mRNA and protein were significantly upregulated in CMECs incubated with ox-LDL. Furthermore, FGF21 levels increased by 200 µmol/L bezafibrate could reduce CMECs apoptosis, and inhibit FGF21 expression by shRNA induced apoptosis (P < 0.05).
Conclusions:
FGF21 may be a signal of injured target tissue, and may play physiological roles in improving the endothelial function at an early stage of atherosclerosis and in stopping the development of coronary heart disease.
Insights
Fibroblast growth factor 21 (FGF21) protects against endothelial dysfunction. This study shows FGF21 reduces apoptosis in cardiac cells damaged by oxidized-low density lipoprotein (ox-LDL), suggesting a role in preventing atherosclerosis.
Area of Science:
- Cardiovascular Research
- Metabolic Regulation
- Endothelial Biology
Background:
- Fibroblast growth factor 21 (FGF21) is a key regulator of glucose and lipid metabolism.
- Atherosclerosis involves endothelial dysfunction and injury.
- The protective role of FGF21 in atherosclerosis requires further investigation.
Purpose of the Study:
- To investigate FGF21's role in preventing atherosclerotic injury and endothelial dysfunction.
- To determine if FGF21 acts as an independent protective factor against atherosclerosis.
Main Methods:
- Assessed FGF21 mRNA and protein levels in cardiac microvascular endothelial cells (CMECs) exposed to oxidized-low density lipoprotein (ox-LDL).
- Investigated the impact of regulating FGF21 expression on CMEC apoptosis.
- Utilized real-time PCR and enzyme-linked immunosorbent assay for FGF21 quantification.
Main Results:
- Ox-LDL significantly upregulated FGF21 mRNA and protein secretion in CMECs.
- Increased FGF21 levels, induced by bezafibrate, reduced CMEC apoptosis.
- Inhibition of FGF21 expression using shRNA led to increased CMEC apoptosis (P < 0.05).
Conclusions:
- FGF21 may serve as a biomarker for injured tissues in atherosclerosis.
- FGF21 appears to play a physiological role in enhancing endothelial function during early atherosclerosis.
- FGF21 may help halt the progression of coronary heart disease.
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