Chemerin as a Driver of Cardiovascular Diseases: New Perspectives and Future Directions

Abstract

In recent years, the immune system has emerged as a key player in the development of atherosclerosis, heart failure, venous thromboembolism, and systemic hypertension. Obesity and related cardiovascular diseases (CVDs) remain the leading global cause of death. Adipokines-hormones produced by adipose tissue-exert diverse endocrine and immunomodulatory effects. Among them, chemerin, discovered in the early 20th century, is a chemotactic molecule that recruits dendritic cells, endothelial cells, macrophages, and lymphocytes during early immune responses. It regulates cell migration and vascular homeostasis. Dysregulated adipokine profiles contribute to chronic inflammation, insulin resistance, metabolic syndrome, and impaired blood pressure control. This review explores chemerin's potential role in CVD pathogenesis, focusing on its immunomodulatory functions, impact on vascular inflammation, and endothelial dysfunction. The presented work also examines recent findings on chemerin's diagnostic and therapeutic potential in cardiovascular health.

Keywords: adipokine; cardiovascular diseases; chemerin; hypertension; obesity.

Figure 1

Figure showing the most important chemerin mechanism of action—the main source of chemerin synthesis is adipose tissue and liver. Chemerin, also known as tazarotene-induced gene (TIG2; RARRES2), acts via three kinds of receptors: CMKLR1 (known also as chemerin 1 or ChemR23) and chemerin 2 (G-protein-coupled receptor 1-GPR1), mediating the direct biological effect of chemerin. In addition, there is a CCRL2, which is described as a chaperone for chemerin. The figure was created in BioRender. Imiela, A.M.

Figure 2

Figure presents the role of perivascular adipose tissue (PVAT) in the pathogenesis of obesity and cardiovascular complications. PVAT serves as a local source of chemerin, which may activate chemerin 1 receptors on sympathetic nerves or smooth muscle cells to promote vascular contraction. Hypertension might lead to endothelial cell injury and activation of endothelial cells’ adhesive molecules, finally promoting atherosclerosis. Higher local chemerin production results in inflammatory cell recruitment and inflammation promotion in white adipose tissue. Obesity and metabolic syndrome development results in poor blood pressure and glycemic control. All the above-mentioned processes promote pro-inflammatory state and contribute to the vicious circle. The figure was created in BioRender. Imiela, A.M.