Printable Handouts

PDF

Navigable Slide Index

1. Introduction
2. Guide to the presentation
3. Inflammation, an inducer and amplifier of diseases
4. Mechanisms contributing to fatty streak formation
5. Mechanisms contributing to lesion progression
6. Mechanisms contributing to unstable lesions
7. Risk factors for the development of atherosclerosis
8. Risk factors and their relationship to inflammation
9. Induction of inflammatory genes
10. Toll like receptors and microbial pathogens
11. Toll like receptors and endogenous ligands
12. TLR4 and its roll in atherosclerosis
13. Modulation of atherosclerosis in mice by TLR2
14. Summary: inflammation and atherosclerosis
15. TLR targets in the nucleus
16. Induction of inflammatory response genes by LPS
17. NCoR co-repressor complexes
18. Conforming the NCoR complex model
19. NCoR complex and signaling pathways
20. Transcriptional control of inflammatory responses
21. Nuclear receptor superfamily
22. Transcriptional activities of nuclear receptors
23. Regulation of the nuclear receptor expression
24. Dexamethasone inhibition
25. Glucocorticoid receptor repression
26. Repression of LPS-responsive genes
27. Nuclear receptors and inflammatory responses
28. PPAR-gamma - structure, function and ligands
29. PPAR-gamma expression in macrophages
30. PPAR-gamma agonists
31. PPAR-gamma ligands and foam cell formation
32. Rosiglitazone inhibition
33. PPAR-gamma ligands and atherosclerotic lesions
34. Effect of Rosiglitazone on markers of inflammation
35. NCoR SUMOylation-dependent mechanism
36. NCoR and PPAR-gamma repression of iNOS
37. NCoR, PPAR-gamma and iNOS
38. Effects of TZDs on cardiovascular risk factors
39. Adverse effects of TZDs
40. PPAR-gamma-specific ligands summary
41. Future prospects
42. 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

Links

Series:

• Innate Immunity

Categories:

• Clinical Practice
• Immunology

Therapeutic Areas:

• Cardiovascular & Metabolic
• Immunology & Inflammation

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 April 15, 2025, from https://doi.org/10.69645/DZYQ8098.
Export Citation (RIS)

Publication History

• Published on May 31, 2009

Financial Disclosures

• Prof. Christopher Glass has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.