What is it about?
The primary objective of this review is to provide a complete and updated overview of the role of HSP60 in different cardiovascular diseases, including the lesser-known and studied, by integrating new studies and investigations done in recent years to the present. Other goals include providing a concise but factual summary of the structure and function of the protein, an outline of its participation in the immune system, and potential therapeutic strategies that have been explored in this area, altogether highlighting its relevance and potential in this specific group of diseases to encourage further research and interest.
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Why is it important?
In the present day, the direct and indirect roles of HSP60 in disease development have been studied extensively in atherosclerosis, heart failure, and some autoimmune diseases. However, in other pathological entities of the spectrum of CVDs, not much research has been done. By presenting a punctual recapitulation of the structure, functions, and roles in immunity of HSP60 and by compiling the knowledge we possess of HSP60 in various CVDs, we believe this review can provide insight into important investigations that have been done in the past and present that shed light to its relevance in disease development and progression. This approach is unique as no comprehensive review of HSP60 in CVDs has been published to the present day. Also, by presenting an executive summary and schematic illustrations of the potential therapeutic targets that have emerged up to the present, we believe we can provide a clear and updated image of the potential course research can take in regards to utilizing this protein as a novel therapeutic strategy for different diseases in the spectrum of CVDs, which altogether encompass an important burden globally.
Perspectives
We believe this work will be a reference to those who are exploring new frontiers wherein this or other cardiometabolic and autoimmune areas, as this protein has the potential to be implemented for either diagnostics or therapeutics in the heart. According to the World Health Organization, cardiovascular diseases (CVD) are the first cause of mortality and morbidity worldwide. It is estimated that by the year 2020, deaths from CVD will increase by 15 to 20% and about 23.6 million people will die from these disorders by 2030, mainly from heart disease and stroke. The pathophysiology behind this spectrum of diseases is very complex and multifactorial. However, inflammation seems to be a common denominator in all of them. Several studies have indicated that heat shock proteins (HSP), a large group of intracellular proteins, play an important role in these processes and can act as either an ally or a foe during disease progression. Specifically, heat shock protein 60 (HSP60), seems to actively participate as a trigger or stressor in various inflammatory states of the cardiovascular system acting as a signaling molecule, a potential role that ultimately favors the development and progression of many CVDs. Interestingly, intracellular HSP60 also possesses various physiological roles necessary for the correct functioning of the cell, including aiding as chaperones, in protein folding and apoptosis. Nonetheless, when found in the extracellular space, HSP60 has both pro-inflammatory and anti-inflammatory roles depending on the interactions with cell-surface receptors including Toll-like receptors (TLRs), while also binding to other proteins during an immune response. As such, the dual role of HSP60 as an immunomodulator and biomarker of damage has allowed researchers to explore different therapeutic strategies targeting this protein and has been an area of interest for many groups throughout the years, and recently, several novel therapeutic targets have come to light in this regard.
Dr. C. Enrique Guerrero-Beltrán
Tecnologico de Monterrey
Read the Original
This page is a summary of: Heat shock protein 60 and cardiovascular diseases: An intricate love‐hate story, Medicinal Research Reviews, August 2020, Wiley,
DOI: 10.1002/med.21723.
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