Alexander N. Neznamov, Yulia P. Baykova and Marina V. Kubekina* Pages 1 - 19 ( 19 )
Monocytes/macrophages play an important role in controlling the onset and progression of inflammatory responses by changing their activation state. Inflammation accompanies some slowly progressing pathologies, such as neurodegenerative diseases, rheumatoid arthritis, atherosclerosis, and other inflammatory disorders. Monocyte/- macrophage differentiation and polarization are accompanied by transcriptional profile changes. A better understanding of the specific ligands and receptors involved in the regulation of immune cell transcription will help to identify selective molecular targets for the therapy of inflammatory diseases. CDKs are key regulators of cell cycle and transcription in eukaryotes. Thus, this review is aimed to examine the role of CDKs in the monocyte-macrophage response and the data obtained from relevant experiments. M1 macrophages can trigger harmful inflammatory responses. A potential solution is to shift the polarization of macrophages towards the protective anti-inflammatory M2 phenotype (macrophage reprogramming). The mechanisms regulating this switch are crucial for the proper functioning of monocytes and macrophages. Inhibition of different types of CDKs leads to changes in the functional activity of monocytes/macrophages. It has been shown that monocytes/macrophage differentiation and immune functions are dependent on CDK activity. Recent studies on CDKs and their role in the immune system have concluded that their activity plays an essential role in monocyte/macrophage differentiation and immune functions. However, the role of CDKs in monocytes, macrophages, and the immune response is not fully understood. Unraveling the role of transcriptional regulators could provide valuable insights for the development of new treatments for macrophage-mediated inflammatory diseases.
Monocytes/macrophages, macrophage immune response, inflammatory diseases, macrophage polarization, cell signaling, CDKs, transcriptional reprogramming.