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Epigenetic regulations of inflammatory cyclooxygenase-derived prostanoids: molecular basis and pathophysiological
1Faculty of Dental Medicine, University of Monastir, 5000 Monastir, Tunisia.
Abstract:
The potential relevance of prostanoid signaling in immunity and immunological disorders, or disease susceptibility and individual variations in drug responses, is an important area for investigation. The deregulation of Cyclooxygenase- (COX-) derived prostanoids has been reported in several immunoinflammatory disorders such as asthma, rheumatoid arthritis, cancer, and autoimmune diseases. In addition to the environmental factors and the genetic background to diseases, epigenetic mechanisms involved in the fine regulation of prostanoid biosynthesis and/or receptor signaling appeared to be an additional level of complexity in the understanding of prostanoid biology and crucial in controlling the different components of the COX pathways. Epigenetic alterations targeting inflammatory components of prostanoid biosynthesis and signaling pathways may be important in the process of neoplasia, depending on the tissue microenvironment and target genes. Here, we focused on the epigenetic modifications of inflammatory prostanoids in physiological immune response and immunological disorders. We described how major prostanoids and their receptors can be functionally regulated epigenetically and consequently the impact of these processes in the pathogenesis inflammatory diseases and the development of therapeutic approaches that may have important clinical applications.
Insights
Epigenetic modifications regulate prostanoid signaling in immune responses and inflammatory diseases. Understanding these epigenetic changes in cyclooxygenase (COX) pathways offers potential for new therapeutic strategies.
Area of Science:
- Immunology and molecular biology, focusing on prostanoid signaling pathways.
Background:
- Prostanoid signaling, particularly from Cyclooxygenase (COX) enzymes, is implicated in various immunoinflammatory disorders like asthma, rheumatoid arthritis, cancer, and autoimmune diseases.
- Epigenetic mechanisms add complexity to prostanoid biology, influencing biosynthesis and receptor signaling, and are crucial for regulating COX pathways.
Purpose of the Study:
- To investigate the role of epigenetic modifications in the regulation of inflammatory prostanoids during physiological immune responses and in immunological disorders.
- To elucidate how epigenetic regulation impacts prostanoid and receptor function and their contribution to inflammatory disease pathogenesis.
Main Methods:
- Review and analysis of existing literature on epigenetic modifications affecting prostanoid biosynthesis and signaling pathways.
- Focus on specific epigenetic alterations impacting inflammatory prostanoids and their receptors in the context of immune function and disease.
Main Results:
- Epigenetic alterations are identified as key regulators of inflammatory prostanoid pathways.
- These modifications influence the function of major prostanoids and their receptors, impacting disease processes.
- Epigenetic control is crucial in the development of inflammatory diseases and potentially in neoplasia.
Conclusions:
- Epigenetic regulation of inflammatory prostanoids is a significant factor in immune homeostasis and disease pathogenesis.
- Understanding these epigenetic mechanisms provides insights into the development of novel therapeutic approaches for inflammatory and immunological disorders.
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