Epigenetics refers to changes in the expression of heritable genes or cellular phenotypes caused by regulating DNA methylation, histone modification, chromatin remodeling, and noncoding RNA expression, without altering the DNA sequence. It plays a critical role in the regulation of many physiological and pathological processes, such as inflammation, immunity, and tumor. In particular, many epigenetic modifiers have been found to affect innate cell development, infection, and inflammatory responses by regulating gene-specific expression. Epigenetic abnormalities often result in changes in gene expression and its function, which in turn promote the process of inflammation and even tumorigenesis.
Autophagy is a highly conserved subcellular degradation process by which some damaged organelles, misfolded proteins, nucleic acids, and pathogenic microorganisms are digested to maintain homeostasis. Autophagy dysregulation has been implicated in multiple diseases, including inflammation, tumors, and neurodegenerative diseases. It is not only a cytoplasmic event, but also involved in the regulation of nuclear components, including histone modifications, microRNA, and transcription factors. Methyltransferase-mediated histone modifications (H3K9me2, H3R17me2, and H3K27me3), miRNAs, and DNA methylation catalyzed by DNA methyltransferase are the key nuclear factors involved in the regulation of autophagy. In addition, some autophagy-related genes (Atgs) promote or inhibit the autophagic process through epigenetic modifications, such as histone modifications and DNA methylation, affecting the occurrence and development of inflammatory diseases. Studying the role of epigenetic regulation of autophagy in inflammatory diseases may help identify novel drug targets and develop potential diagnostic and therapeutic approaches. Although the biological and clinical significance of epigenetic modification of autophagy has attracted more and more attention from researchers, this regulation is very complex and its role and mechanism in inflammatory diseases are still unclear.
This Research Topic aims to explore the regulatory function and mechanism of epigenetic modifications of autophagy in inflammatory diseases and the potential of using epigenetic and autophagy-targeting compounds to prevent and treat inflammatory diseases, especially cancer, inflammatory bowel disease, rheumatoid arthritis, viral infections, etc. Meanwhile, the aim of this Topic is to present the advances in understanding the function, mechanism, and immunomodulatory effects of epigenetic modifications of autophagy in inflammatory diseases, as well as the latest progress in the development of drugs targeting epigenetics and autophagy.
We encourage the submission of Original Research articles, Perspectives, Clinical Trials, Reviews, and Mini-Reviews covering, but not limited to, the following subtopics:
1) Regulatory function of epigenetic modifications of autophagy in inflammatory diseases;
2) Signaling pathways of epigenetic modification of autophagy in inflammatory diseases;
3) Role of epigenetic modifications in different types of autophagy, e.g. macroautophagy, microautophagy, and chaperone-mediated autophagy (CMA) in inflammation and immunity;
4) Role of epigenetics in regulating senescence-associated secretory phenotype (SASP) in the context of immunity;
5) Molecular mechanisms of immune cells in affecting epigenetic modification of autophagy in the context of inflammation;
6) Development of new targeted therapies for the treatment of inflammatory diseases.
Epigenetics refers to changes in the expression of heritable genes or cellular phenotypes caused by regulating DNA methylation, histone modification, chromatin remodeling, and noncoding RNA expression, without altering the DNA sequence. It plays a critical role in the regulation of many physiological and pathological processes, such as inflammation, immunity, and tumor. In particular, many epigenetic modifiers have been found to affect innate cell development, infection, and inflammatory responses by regulating gene-specific expression. Epigenetic abnormalities often result in changes in gene expression and its function, which in turn promote the process of inflammation and even tumorigenesis.
Autophagy is a highly conserved subcellular degradation process by which some damaged organelles, misfolded proteins, nucleic acids, and pathogenic microorganisms are digested to maintain homeostasis. Autophagy dysregulation has been implicated in multiple diseases, including inflammation, tumors, and neurodegenerative diseases. It is not only a cytoplasmic event, but also involved in the regulation of nuclear components, including histone modifications, microRNA, and transcription factors. Methyltransferase-mediated histone modifications (H3K9me2, H3R17me2, and H3K27me3), miRNAs, and DNA methylation catalyzed by DNA methyltransferase are the key nuclear factors involved in the regulation of autophagy. In addition, some autophagy-related genes (Atgs) promote or inhibit the autophagic process through epigenetic modifications, such as histone modifications and DNA methylation, affecting the occurrence and development of inflammatory diseases. Studying the role of epigenetic regulation of autophagy in inflammatory diseases may help identify novel drug targets and develop potential diagnostic and therapeutic approaches. Although the biological and clinical significance of epigenetic modification of autophagy has attracted more and more attention from researchers, this regulation is very complex and its role and mechanism in inflammatory diseases are still unclear.
This Research Topic aims to explore the regulatory function and mechanism of epigenetic modifications of autophagy in inflammatory diseases and the potential of using epigenetic and autophagy-targeting compounds to prevent and treat inflammatory diseases, especially cancer, inflammatory bowel disease, rheumatoid arthritis, viral infections, etc. Meanwhile, the aim of this Topic is to present the advances in understanding the function, mechanism, and immunomodulatory effects of epigenetic modifications of autophagy in inflammatory diseases, as well as the latest progress in the development of drugs targeting epigenetics and autophagy.
We encourage the submission of Original Research articles, Perspectives, Clinical Trials, Reviews, and Mini-Reviews covering, but not limited to, the following subtopics:
1) Regulatory function of epigenetic modifications of autophagy in inflammatory diseases;
2) Signaling pathways of epigenetic modification of autophagy in inflammatory diseases;
3) Role of epigenetic modifications in different types of autophagy, e.g. macroautophagy, microautophagy, and chaperone-mediated autophagy (CMA) in inflammation and immunity;
4) Role of epigenetics in regulating senescence-associated secretory phenotype (SASP) in the context of immunity;
5) Molecular mechanisms of immune cells in affecting epigenetic modification of autophagy in the context of inflammation;
6) Development of new targeted therapies for the treatment of inflammatory diseases.