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Printable Handouts
Navigable Slide Index
- Introduction
- Guide to the presentation
- Inflammation, an inducer and amplifier of diseases
- Mechanisms contributing to fatty streak formation
- Mechanisms contributing to lesion progression
- Mechanisms contributing to unstable lesions
- Risk factors for the development of atherosclerosis
- Risk factors and their relationship to inflammation
- Induction of inflammatory genes
- Toll like receptors and microbial pathogens
- Toll like receptors and endogenous ligands
- TLR4 and its roll in atherosclerosis
- Modulation of atherosclerosis in mice by TLR2
- Summary: inflammation and atherosclerosis
- TLR targets in the nucleus
- Induction of inflammatory response genes by LPS
- NCoR co-repressor complexes
- Conforming the NCoR complex model
- NCoR complex and signaling pathways
- Transcriptional control of inflammatory responses
- Nuclear receptor superfamily
- Transcriptional activities of nuclear receptors
- Regulation of the nuclear receptor expression
- Dexamethasone inhibition
- Glucocorticoid receptor repression
- Repression of LPS-responsive genes
- Nuclear receptors and inflammatory responses
- PPAR-gamma - structure, function and ligands
- PPAR-gamma expression in macrophages
- PPAR-gamma agonists
- PPAR-gamma ligands and foam cell formation
- Rosiglitazone inhibition
- PPAR-gamma ligands and atherosclerotic lesions
- Effect of Rosiglitazone on markers of inflammation
- NCoR SUMOylation-dependent mechanism
- NCoR and PPAR-gamma repression of iNOS
- NCoR, PPAR-gamma and iNOS
- Effects of TZDs on cardiovascular risk factors
- Adverse effects of TZDs
- PPAR-gamma-specific ligands summary
- Future prospects
- Acknowledgements
Topics Covered
- Nuclear receptors comprise a superfamily of ligand- and signal-dependent transcription factors that regulate diverse aspects of reproduction, development, metabolism and immunity
- Recent studies have demonstrated that a subset of nuclear receptors can co-ordinately regulate aspects of inflammation and metabolism that impact on the development of atherosclerosis and type 2 diabetes by inhibiting transcriptional responses to toll like receptors
- The nuclear receptor co-repressor NCoR plays a key role in maintaining inflammatory response genes in a repressed state under basal conditions
- PPARg inhibits inflammatory responses by preventing the removal of NCoR from target genes
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Talk Citation
Glass, C. (2009, May 31). Nuclear receptors at the crossroads of inflammation and atherosclerosis [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved October 13, 2024, from https://doi.org/10.69645/DZYQ8098.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Christopher Glass has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
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