{"title":"The Role of Autophagy and Macrophage Polarization in the Process of Chronic Inflammation and Regeneration","authors":"S. G. Zubova, A. V. Morshneva","doi":"10.1134/s1990519x24700184","DOIUrl":null,"url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>Many serious illnesses, including diabetes, obesity, osteoporosis, and neurodegenerative diseases, are caused by chronic inflammation that develops in fat tissue, bones, or the brain. This inflammation occurs due to a shift in macrophage (microglia) polarization toward a proinflammatory M1 phenotype. It has now been proven that macrophage polarization is determined by the intracellular level of autophagy in the macrophage. By modulating autophagy, it is possible to cause a switch in macrophage activity towards M1 or M2. Summarizing the material accumulated in the literature, we believe that activation of autophagy reprograms the macrophage towards M2, replacing its protein content and receptor apparatus, and activate a another type of metabolism. The term “reprogramming” is most appropriate for this process, since it is followed by a change in the functional activity of the macrophage, namely a switch from cytotoxic proinflammatory activity to anti-inflammatory (regenerative) activity. Modulation of autophagy may be an approach to the treatment of cancer, neurodegenerative disorders, osteoporosis, diabetes and other serious diseases.</p>","PeriodicalId":9705,"journal":{"name":"Cell and Tissue Biology","volume":"22 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cell and Tissue Biology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1134/s1990519x24700184","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Biochemistry, Genetics and Molecular Biology","Score":null,"Total":0}
引用次数: 0
Abstract
Many serious illnesses, including diabetes, obesity, osteoporosis, and neurodegenerative diseases, are caused by chronic inflammation that develops in fat tissue, bones, or the brain. This inflammation occurs due to a shift in macrophage (microglia) polarization toward a proinflammatory M1 phenotype. It has now been proven that macrophage polarization is determined by the intracellular level of autophagy in the macrophage. By modulating autophagy, it is possible to cause a switch in macrophage activity towards M1 or M2. Summarizing the material accumulated in the literature, we believe that activation of autophagy reprograms the macrophage towards M2, replacing its protein content and receptor apparatus, and activate a another type of metabolism. The term “reprogramming” is most appropriate for this process, since it is followed by a change in the functional activity of the macrophage, namely a switch from cytotoxic proinflammatory activity to anti-inflammatory (regenerative) activity. Modulation of autophagy may be an approach to the treatment of cancer, neurodegenerative disorders, osteoporosis, diabetes and other serious diseases.
期刊介绍:
The journal publishes papers on vast aspects of cell research, including morphology, biochemistry, biophysics, genetics, molecular biology, immunology. The journal accepts original experimental studies, theoretical articles suggesting novel principles and approaches, presentations of new hypotheses, reviews highlighting major developments in cell biology, discussions. The main objective of the journal is to provide a competent representation and integration of research made on cells (animal and plant cells, both in vivo and in cell culture) offering insight into the structure and functions of live cells as a whole. Characteristically, the journal publishes articles on biology of free-living and parasitic protists, which, unlike Metazoa, are eukaryotic organisms at the cellular level of organization.