Role of Heat Shock Protein 27 in Modulating Atherosclerotic Inflammation

Atherosclerosis is the primary cause of heart attacks, and while efforts to prevent its development or progression have historically focused largely on reducing cholesterol levels, there is now important proof-of-principle data that supports the role that inflammation plays in atherogenesis. Heat sh...

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Bibliographic Details
Published in:Journal of cardiovascular translational research 2021-02, Vol.14 (1), p.3-12
Main Authors: Inia, Jose A., O’Brien, Edward R.
Format: Article
Language:English
Subjects:
Biomedical Engineering and Bioengineering
Biomedicine
Cardiology
Human Genetics
Medicine
Medicine & Public Health
Review Article
Special Issue: Immunomodulation
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Summary:Atherosclerosis is the primary cause of heart attacks, and while efforts to prevent its development or progression have historically focused largely on reducing cholesterol levels, there is now important proof-of-principle data that supports the role that inflammation plays in atherogenesis. Heat shock protein 27 (HSP27) is a novel biomarker of atherosclerosis that is also atheroprotective. Through a series of murine and in vitro experiments, an iterative narrative is emerging that demonstrates how HSP27 can act as an extracellular mediator that reduces plaque inflammation—either directly via transcriptional pathways, or indirectly via important effects on macrophage biology. While there is much more to learn about the biology of HSP27, we now review the strong foundation of knowledge that highlights the potential anti-inflammatory role of HSP27 as a novel therapeutic for not only atherosclerosis but potentially other inflammatory disorders.
ISSN:1937-5387
1937-5395
DOI:10.1007/s12265-020-10000-z