Published online Mar 6, 2022. doi: 10.12998/wjcc.v10.i7.2095
Peer-review started: August 28, 2021
First decision: November 17, 2021
Revised: December 1, 2021
Accepted: January 22, 2022
Article in press: January 22, 2022
Published online: March 6, 2022
Processing time: 185 Days and 17.1 Hours
Lipid metabolism plays an essential role in the pathogenesis of atherosclerosis, a major cause for coronary heart disease (CHD). Lipid regulation therapy can reduce major adverse cardiovascular events. Although previous studies have shown that betatrophin, angiogenin-like protein 3 and lipoprotein lipase are jointly involved in lipid regulation, the interaction and mechanism of action between them are still controversial.
The purpose of this study was to explore the correlation between the betatrophin/ angiogenin-likeprotein3 (ANGPTL3) / lipoprotein lipase (LPL) pathway and severity of coronary artery disease in patients with CHD. The detection of this pathway in CHD patients with acute coronary occlusion may have more diagnostic value. Betatrophin can also be used as a target for new lipid regulation treatments to provide clues for the development of new drugs.
The betatrophin/ANGPTL3/LPL pathway is related to the severity of CHD. In addition, the results showed that the levels of LPL and ANGPTL3 in CHD patients increased, and their increasing trends were consistent. The detection of this pathway can be used as one of the non-invasive tools to evaluate the severity of coronary artery disease (CAD) lesions in patients with CHD. Not only that, betatrophin may also serve as a new target for lipid regulation therapy.
This case–control study involved 277 individuals. Nondiabetic patients diagnosed with CHD were selected as the case group; 79 were of Kazakh descent and 72 were of Han descent. The control groups comprised of 61 Kazakh and 65 Han individuals. The serum levels of betatrophin and LPL were detected by enzyme-linked immunosorbent assay (ELISA), and the double antibody sandwich ELISA was used to detect serum level of ANGPTL3. The data are expressed as average ± standard deviation, and the statistical differences between the data were compared by independent sample t-test. Differences between groups were analyzed by two-way analysis of variance, multigroup analysis of variance, correlation analysis by Spearman correlation, and risk factor assessment by ordered logistic regression analysis.
The betatrophin/ANGPTL3/LPL pathway is positively correlated with the severity of CAD. The levels of serum betatrophin and ANGPTL3 in the Kazakh CHD group with severe CAD were significantly higher than those in the Han CHD group with severe CAD. However, there was no significant difference in serum LPL levels in patients with mild CAD. Logistic regression analysis revealed that TG and serum betatrophin were risk factors for coronary atherosclerosis in Kazakh patients, and BMI and serum betatrophin were risk factors for coronary atherosclerosis in Han patients. Other expression mechanisms of betatrophin in lipid regulation still need to be explored. The inflammatory response and autophagy mediated by betatrophin in atherosclerosis may become a new research direction.
There was a correlation between the betatrophin/ANGPTL3/LPL pathway and severity of CAD in patients with CHD.
The expression of betatrophin in other tissues and its new mechanism of lipid regulation, as well as the inflammatory response and autophagy of atherosclerosis mediated by betatrophin may become new research directions. Not only that, betatrophin can also be used as a target for new lipid regulation treatments to provide clues for the development of new drugs.