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RESEARCH ARTICLE

New Horizons in the Study of WNT and JAK/STAT Signaling Pathways in Cardiometabolic Diseases

The Open Biomarkers Journal 01 Nov 2024 RESEARCH ARTICLE DOI: 10.2174/0118753183297843240905081014

Abstract

Aim

Despite advances in diagnosis and treatment, cardiometabolic diseases remain a major worldwide health problem. A new direction in identifying biomarkers that increase diagnostics predictive potential is the study of the WNT and JAK/STAT signaling pathways. Experimental and clinical studies have provided mixed evidence that determined the purpose of the study. This study aimed to examine the characteristics of the production of certain JAK/STAT and WNT signaling proteins in cardiometabolic pathology patients.

Materials and Methods

The research involved patients with myocardial infarction and cardiometabolic syndrome, as well as healthy individuals. Measurement of proteins STAT-1, STAT-3, STAT-6, β-catenin, sclerostin, WIF-1, GSK-3 α, and β, DVL-1 serum concentrations was carried out by ELISA.

Results

We established a wide range of JAK/STAT and WNT signaling protein values in the patient’s blood serum. In cardiometabolic syndrome, there was an increase in the concentrations of β-catenin, DVL-1, GSK-3α, and GSK-3β and a decrease in STAT-1, 3, compared with healthy individuals. During myocardial infarction, an increase in β-catenin, WIF-1, and DVL-1 and a decrease in sclerostin, GSK-3α, STAT-1, STAT-3, and STAT-6 were recorded compared with healthy individuals. The most significant intergroup differences were found for β-catenin, WIF -1, DVL-1, GSK-3α and STAT-6. Statistically significant correlations between the levels of a number of JAK/STAT and WNT signaling proteins and lipid profile parameters were revealed.

Conclusion

The data received about changes in the production of proteins of the WNT and JAK/STAT signaling pathways expand the molecular mechanisms of cardiometabolic diseases' immunopathogenesis understanding.

Keywords: Cardiometabolic diseases, Myocardial infarction, WNT signaling pathway, JAK/STAT signaling, Coronary heart disease, Immunopathogenesis.
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