Inflammation is a response of the human body to various noxious internal and external stimuli, including an array of infectious (pathogens) or other non-infectious (including damaged cell or toxic compounds) agents. Acute inflammation is often a healing mechanism that aids in maintaining tissue homeostasis during infection and injury and is tightly regulated. However, unresolved inflammation may lead to chronic inflammation by maintaining low levels of pro-inflammatory cytokines and other inflammatory mediators, affecting multiple organs and resulting in tissue damage or disease-states by activating specific signaling axes. Chronic inflammation originating in the immune, epithelial and stromal compartment has been a major driver of aging and age-related diseases, including auto-immune diseases, neurodegeneration, cardiovascular disease, diabetes mellitus, and cancer, driving disability and mortality worldwide. Infact, almost 25% of human cancers have been shown to result from chronic inflammation. Recent advances in whole-genome sequencing have highlighted the role of epigenetic modulation of the various inflammatory genes involved in promoting aging, termed inflamm-aging, as well as age-related diseases. Epigenetic modifications like hypermethylation of CpG islands, demethylation, acetylation, loss of heterochromatic marks all have been demonstrated to drive these pathogenetic mechanisms. In the context of cancer, the importance of such modification is further highlighted, given the demethylation of certain inflammatory mediators, genes can dictate the tumor stage, metastasis, and overall survival of cancer patients. Collectively, the above pieces of evidence highlight an urgent need to understand the role of epigenetic regulators in the pathogenesis of such diseases to develop therapeutic interventions. Brief background information on the area of research to give context to the Research Topic.
Chronic inflammation plays an important role in driving both inflammatory diseases associated with aging including cancer. Recent advances have been made towards the understanding of how such inflammation may drive diseases. However knowledge related to how epigenetic mechanisms may drive the generation of such diseases in various stromal, immune and epithelial compartments remain limited. The goal of this research topic would be to shed light on mechanisms by which the plethora of epigenetic regulators may mediate histone modifications and drive such disease states. We will focus on the various groups enzymes classified as DNA and histone methyl transferases, demethylases, histone acetyl transferases and histone deacetylases and others that drive modifications in histone and DNA that reprograms the epigenome to reprogram the transcriptome, metabolome and proteome of the cells and incite inflammatory diseases.
• Epigenetic regulation of specific pathways in various cell types of the epithelia and the stroma and how these pathways relate to diseases.
• Epigenetic regulation of pathways leading to chronic inflammatory states
• Epigenetic regulation of molecular pathways that may affect disease initiation
• Epigenetic regulation of immune pathways in the immune compartment specifically that may deregulate the immune system and drive diseases
Inflammation is a response of the human body to various noxious internal and external stimuli, including an array of infectious (pathogens) or other non-infectious (including damaged cell or toxic compounds) agents. Acute inflammation is often a healing mechanism that aids in maintaining tissue homeostasis during infection and injury and is tightly regulated. However, unresolved inflammation may lead to chronic inflammation by maintaining low levels of pro-inflammatory cytokines and other inflammatory mediators, affecting multiple organs and resulting in tissue damage or disease-states by activating specific signaling axes. Chronic inflammation originating in the immune, epithelial and stromal compartment has been a major driver of aging and age-related diseases, including auto-immune diseases, neurodegeneration, cardiovascular disease, diabetes mellitus, and cancer, driving disability and mortality worldwide. Infact, almost 25% of human cancers have been shown to result from chronic inflammation. Recent advances in whole-genome sequencing have highlighted the role of epigenetic modulation of the various inflammatory genes involved in promoting aging, termed inflamm-aging, as well as age-related diseases. Epigenetic modifications like hypermethylation of CpG islands, demethylation, acetylation, loss of heterochromatic marks all have been demonstrated to drive these pathogenetic mechanisms. In the context of cancer, the importance of such modification is further highlighted, given the demethylation of certain inflammatory mediators, genes can dictate the tumor stage, metastasis, and overall survival of cancer patients. Collectively, the above pieces of evidence highlight an urgent need to understand the role of epigenetic regulators in the pathogenesis of such diseases to develop therapeutic interventions. Brief background information on the area of research to give context to the Research Topic.
Chronic inflammation plays an important role in driving both inflammatory diseases associated with aging including cancer. Recent advances have been made towards the understanding of how such inflammation may drive diseases. However knowledge related to how epigenetic mechanisms may drive the generation of such diseases in various stromal, immune and epithelial compartments remain limited. The goal of this research topic would be to shed light on mechanisms by which the plethora of epigenetic regulators may mediate histone modifications and drive such disease states. We will focus on the various groups enzymes classified as DNA and histone methyl transferases, demethylases, histone acetyl transferases and histone deacetylases and others that drive modifications in histone and DNA that reprograms the epigenome to reprogram the transcriptome, metabolome and proteome of the cells and incite inflammatory diseases.
• Epigenetic regulation of specific pathways in various cell types of the epithelia and the stroma and how these pathways relate to diseases.
• Epigenetic regulation of pathways leading to chronic inflammatory states
• Epigenetic regulation of molecular pathways that may affect disease initiation
• Epigenetic regulation of immune pathways in the immune compartment specifically that may deregulate the immune system and drive diseases