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Published on: September 15, 2017
Nuclear receptors and inflammation control: molecular mechanisms and pathophysiological relevance
Wendy Huang1, Christopher K Glass
1Department of Cellular and Molecular Medicine, Department of Medicine, University of California, San Diego, La Jolla, CA, USA.
Abstract:
Tissue inflammation is a tightly regulated process that normally serves to recruit the immune system to sites of infection and injury and to facilitate tissue repair processes. When an inflammatory state is excessive or prolonged, local and systemic damage to host tissues can result in loss of normal physiological functions. Here, we briefly review recent studies that advance our understanding of signaling pathways involved in initiation of inflammatory responses at the level of transcription and counterregulation of these pathways by selected members of the nuclear receptor superfamily. Studies of the intersection of nuclear receptors and inflammation have revealed mechanisms of positive and negative transcriptional control that may provide new targets for pharmacological intervention in chronic diseases, such as atherosclerosis.
Insights
Inflammation is a normal immune response, but prolonged inflammation causes tissue damage. Nuclear receptors offer potential therapeutic targets for chronic inflammatory diseases like atherosclerosis.
Area of Science:
- Immunology
- Molecular Biology
- Pharmacology
Background:
- Tissue inflammation is a critical immune process for host defense and repair.
- Dysregulated or chronic inflammation leads to significant tissue damage and loss of function.
- Nuclear receptors play a role in regulating inflammatory signaling pathways.
Purpose of the Study:
- To review recent studies on signaling pathways in inflammatory response initiation.
- To explore the role of nuclear receptors in counterregulating inflammation.
- To identify potential pharmacological targets for chronic inflammatory diseases.
Main Methods:
- Review of recent scientific literature.
- Analysis of transcriptional regulation in inflammation.
- Investigation of nuclear receptor superfamily functions.
Main Results:
- Signaling pathways at the transcriptional level initiate inflammatory responses.
- Nuclear receptors modulate these inflammatory pathways.
- Mechanisms of positive and negative transcriptional control are elucidated.
Conclusions:
- Understanding nuclear receptor-inflammation interactions reveals key regulatory mechanisms.
- These mechanisms offer novel therapeutic targets for chronic inflammatory conditions such as atherosclerosis.
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