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Published on: September 22, 2019
From signals to systems: the epigenetic-microbiome-mitochondrial axis in IBD pathogenesis
Nesa Kazemifard1, Shabnam Shahrokh1, Georges Dimitrov2,3
1Research Institute for Gastroenterology and Liver Diseases (RIGLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Inflammatory bowel disease (IBD) involves complex interactions between genetics, environment, and the gut microbiome. Understanding the microbiome-epigenome-mitochondrial axis offers new precision strategies for IBD treatment.
Area of Science:
- Gastroenterology and Immunology
- Microbiome Research
- Epigenetics
Background:
- Inflammatory bowel disease (IBD) is increasingly viewed as a systems-level condition.
- It arises from interactions among host genetics, environment, gut microbiome, and epigenetics.
- Epigenetic mechanisms integrate environmental and microbial signals into immune and tissue repair pathways.
Purpose of the Study:
- To synthesize emerging insights into the microbiome-epigenome-mitochondrial axis in IBD.
- To propose a conceptual framework for understanding IBD pathogenesis.
- To discuss potential for biomarker discovery and therapeutic innovation.
Main Methods:
- Review of current scientific literature on IBD, epigenetics, and the microbiome.
- Synthesis of data on microbial metabolites and their impact on host epigenetics and metabolism.
- Integration of findings into a conceptual framework.
Main Results:
- Intestinal dysbiosis and microbial metabolites (e.g., SCFAs, bile acids) alter host metabolism and chromatin states.
- A bidirectional microbiome-epigenome dialogue influences mucosal homeostasis or drives inflammation.
- The microbiome-epigenome-mitochondrial axis is a key player in IBD pathogenesis.
Conclusions:
- An integrative perspective on the microbiome-epigenome-mitochondrial axis is crucial for understanding IBD.
- This framework can guide biomarker discovery and the development of novel therapies.
- Targeting this axis may lead to precision strategies for restoring mucosal equilibrium in IBD.
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