About this Research Topic
Immunopathology of Non-Infectious Inflammatory Diseases: Focus on Genetics and Epigenetics of Atherosclerosis
Inflammation is a natural defensive response of the immune system to what it considers pathogenic. When regulation of inflammatory response is violated, chronic inflammation may develop which is at the origin of multiple diseases and pathological conditions such as neurodegenerative disorders, cancer, metabolic syndrome, autoimmune diseases, atherosclerosis and aging. We are still very far from a complete understanding of all pathological factors and changes leading to chronic inflammation, including corresponding genetic and epigenetic changes.
The goal of this research topic is to collect and summarize recent findings related to the role of genes, mutations, genetic interactions and epigenetic changes in the development of non-infectious inflammatory diseases, with a focus specifically on atherosclerosis. The complete details of pathogenesis of this disease are still unknown. Atherosclerosis is considered as an inflammatory disease involving or being affected by almost all spectra of immune cells related to inborn and adaptive immunity. Despite certain progress in treatment of atherosclerosis mainly by lipid-lowering therapy, the lack of understanding of roots of this disease makes the creation of effective therapy almost impossible.
The main idea of this Research Topic is to combine studies on the genetics of immunopathology of atherosclerosis and other non-infectious inflammatory diseases, chronic inflammation, immunomodulatory activity of the microbiome, autoimmune diseases, and effects of drugs and natural substances on genes and gene networks in the case of above mentioned diseases. Better understanding of underlying pathological mechanisms will allow us to reveal future pharmacological targets for therapy of atherosclerosis and other chronic inflammatory diseases and improve current therapeutic approaches.
The aim of the topic is to provide a collection of multidisciplinary research, review articles, together with clinical studies, addressing genetic and epigenetic aspects of immunopathology of atherosclerosis and other non-infectious inflammatory diseases, that includes, but is not limited to the following:
genetics of immunopathology of atherosclerosis.
immunogenetics of non-infectious inflammatory diseases.
epigenetic changes upon atherosclerosis.
epigenetic mechanisms of regulation of inflammation.
genetic and epigenetic changes in monocytes, macrophages, T- and B-cells, smooth muscle cells, endothelial cells upon atherosclerosis
genetic and epigenetic changes in monocytes, macrophages, T- and B-cells, endothelial cells related to the regulation of lipid metabolism (with the focus on the mechanism of cholesterol accumulation induced by atherogenic LDL)
identification of gene networks contributing to inflammation development.
the search of pharmacological targets for atherosclerosis therapy: genetics and epigenetics aspects.
the development of novel anti-inflammatory therapies.
Manuscripts covering pure bioinformatic analyses are not in scope of the Immunogenetics section of Frontiers in Genetics. Experimental (wet lab) validation of the in silico obtained results is prerequisite for peer-review. Further, reports oriented towards application of genetic analyses in oncological disease are not to be primarily targeted to the Immunogenetics unless they evolve in detail around the MHC (HLA) or other major immunogenetic systems and how those affect immune response and or therapy documented by real laboratory and/or clinical data, not solely bioinformatic analyses.
Inflammation is a natural defensive response of the immune system to what it considers pathogenic. When regulation of inflammatory response is violated, chronic inflammation may develop which is at the origin of multiple diseases and pathological conditions such as neurodegenerative disorders, cancer, metabolic syndrome, autoimmune diseases, atherosclerosis and aging. We are still very far from a complete understanding of all pathological factors and changes leading to chronic inflammation, including corresponding genetic and epigenetic changes.
The goal of this research topic is to collect and summarize recent findings related to the role of genes, mutations, genetic interactions and epigenetic changes in the development of non-infectious inflammatory diseases, with a focus specifically on atherosclerosis. The complete details of pathogenesis of this disease are still unknown. Atherosclerosis is considered as an inflammatory disease involving or being affected by almost all spectra of immune cells related to inborn and adaptive immunity. Despite certain progress in treatment of atherosclerosis mainly by lipid-lowering therapy, the lack of understanding of roots of this disease makes the creation of effective therapy almost impossible.
The main idea of this Research Topic is to combine studies on the genetics of immunopathology of atherosclerosis and other non-infectious inflammatory diseases, chronic inflammation, immunomodulatory activity of the microbiome, autoimmune diseases, and effects of drugs and natural substances on genes and gene networks in the case of above mentioned diseases. Better understanding of underlying pathological mechanisms will allow us to reveal future pharmacological targets for therapy of atherosclerosis and other chronic inflammatory diseases and improve current therapeutic approaches.
The aim of the topic is to provide a collection of multidisciplinary research, review articles, together with clinical studies, addressing genetic and epigenetic aspects of immunopathology of atherosclerosis and other non-infectious inflammatory diseases, that includes, but is not limited to the following:
genetics of immunopathology of atherosclerosis.
immunogenetics of non-infectious inflammatory diseases.
epigenetic changes upon atherosclerosis.
epigenetic mechanisms of regulation of inflammation.
genetic and epigenetic changes in monocytes, macrophages, T- and B-cells, smooth muscle cells, endothelial cells upon atherosclerosis
genetic and epigenetic changes in monocytes, macrophages, T- and B-cells, endothelial cells related to the regulation of lipid metabolism (with the focus on the mechanism of cholesterol accumulation induced by atherogenic LDL)
identification of gene networks contributing to inflammation development.
the search of pharmacological targets for atherosclerosis therapy: genetics and epigenetics aspects.
the development of novel anti-inflammatory therapies.
Manuscripts covering pure bioinformatic analyses are not in scope of the Immunogenetics section of Frontiers in Genetics. Experimental (wet lab) validation of the in silico obtained results is prerequisite for peer-review. Further, reports oriented towards application of genetic analyses in oncological disease are not to be primarily targeted to the Immunogenetics unless they evolve in detail around the MHC (HLA) or other major immunogenetic systems and how those affect immune response and or therapy documented by real laboratory and/or clinical data, not solely bioinformatic analyses.
Keywords: Chronic Inflammation, Genetics, Epigenetics, Immunity, Atherosclerosis
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
