The research team led by Professor Youngkeun Ahn from the Department of Cardiology at Chonnam National University Hospital has discovered a new therapeutic target for the prevention of atherosclerosis, opening up new possibilities in the treatment of cardiovascular diseases.
On August 25, Professor Youngkeun Ahn and Research Professor Yong Sook Kim from the Biomedical Research Institute announced that they had identified the 'ANGPTL4 protein' as a new therapeutic target that prevents atherosclerosis by preserving the function of vascular endothelial cells. The research team clarified the mechanism by which the 'ANGPTL4 protein' stabilizes KLF2, a key regulatory factor in vascular endothelial cells, thereby protecting vascular health.
This study, titled "ANGPTL4 prevents atherosclerosis by preserving KLF2 to suppress EndMT and mitigates endothelial dysfunction" (First author: Dongim Cho, Chonnam National University Cell Regeneration Center; Corresponding authors: Youngkeun Ahn and Yong Sook Kim), was published online in "Arteriosclerosis, Thrombosis, and Vascular Biology," the most prestigious journal issued by the American Heart Association.
Endothelial cells lining the inner wall of blood vessels play a vital role in maintaining vascular health by dilating blood vessels and preventing thrombosis. When endothelial cell function is impaired due to hypertension, diabetes, or hyperlipidemia, blood vessels constrict and inflammation is promoted, marking the onset of atherosclerosis. In particular, when the phenomenon of endothelial-to-mesenchymal transition (EndMT) occurs, in which endothelial cells transform into muscle cells, atherosclerosis accelerates.
The research team administered ANGPTL4 to a mouse model of atherosclerosis and confirmed that ANGPTL4 maintains the expression and function of KLF2, the key regulatory factor of vascular endothelial cells, thereby preserving the unique characteristics of endothelial cells. Furthermore, an analysis of human coronary atherosclerotic plaques revealed that in unstable plaques, the unique characteristics of endothelial cells were lost and KLF2 expression was significantly reduced, supporting the findings from the animal experiments.
Even more noteworthy are the results of the clinical analysis conducted on patients with myocardial infarction. It was found that the lower the blood concentration of ANGPTL4 in patients, the higher the risk of endothelial dysfunction, suggesting that ANGPTL4 could serve as an important indicator of cardiovascular health.
Professor Youngkeun Ahn stated, "This study is significant in that it presents a new mechanism by which the ANGPTL4-KLF2 axis suppresses endothelial-to-mesenchymal transition and protects vascular endothelial function. ANGPTL4 could become a new therapeutic target for atherosclerosis and endothelial dysfunction."
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