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Role of Heat Shock Protein 27 in Modulating Atherosclerotic Inflammation

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Abstract

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.

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Funding

This manuscript was supported by research grants to E.R. O’Brien from the Canadian Institutes of Health Research (CIHR; ISO-110836 & PJT-149015), by an Advancing Science Through Pfizer-Investigator Research Exchange (ASPIRE; WI218510) Cardiovascular Grant, and through the generous research funding support from Libin Cardiovascular Institute.

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Correspondence to Edward R. O’Brien.

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All procedures performed in human studies performed by the O’Brien laboratory and cited in this review manuscript were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards.

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Inia, J.A., O’Brien, E.R. Role of Heat Shock Protein 27 in Modulating Atherosclerotic Inflammation. J. of Cardiovasc. Trans. Res. 14, 3–12 (2021). https://doi.org/10.1007/s12265-020-10000-z

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