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Heat shock protein 60 and cardiovascular diseases: An intricate love-hate story
Indumathi Krishnan-Sivadoss1, Iván A Mijares-Rojas1, Ramiro A Villarreal-Leal1
1Tecnologico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Medicina Cardiovascular y Metabolómica, Monterrey, Nuevo León, México.
Insights
Heat shock protein 60 (HSP60) plays a dual role in cardiovascular diseases (CVDs), offering protection yet potentially driving inflammation. Targeting HSP60 shows promise as a therapeutic strategy for CVDs.
Area of Science:
- Cardiovascular biology
- Immunology
- Molecular medicine
Background:
- Cardiovascular diseases (CVDs) stem from complex pathophysiological processes affecting the heart and blood vessels.
- Inflammation, triggered by cellular stress (apoptosis, oxidative stress), is a primary driver of cardiovascular dysfunction.
- Heat shock protein 60 (HSP60) acts as an intracellular chaperone with a dual role in cardiovascular homeostasis.
Purpose of the Study:
- To review the multifaceted functions of HSP60 in cellular and immune regulation.
- To explore the implications of HSP60 in the development and progression of CVDs.
- To summarize therapeutic strategies targeting HSP60 for cardiovascular and other diseases.
Main Methods:
- Literature review of studies on HSP60.
- Analysis of HSP60's role in cellular stress responses.
- Examination of HSP60's involvement in innate and adaptive immunity.
Main Results:
- HSP60 can protect against cellular injury but also initiate damaging immune responses.
- HSP60 is implicated in the pathogenesis and advancement of cardiovascular diseases.
- Studies indicate HSP60 targeting as a potential therapeutic avenue.
Conclusions:
- HSP60's complex role necessitates careful consideration for therapeutic interventions.
- Targeting HSP60 may offer novel treatment options for cardiovascular conditions.
- Further research is warranted to fully elucidate HSP60's therapeutic potential.
Abstract:
Cardiovascular diseases (CVDs) are the result of complex pathophysiological processes in the tissues comprising the heart and blood vessels. Inflammation is the main culprit for the development of cardiovascular dysfunction, and it may be traced to cellular stress events including apoptosis, oxidative and shear stress, and cellular and humoral immune responses, all of which impair the system's structure and function. An intracellular chaperone, heat shock protein 60 (HSP60) is an intriguing example of a protein that may both be an ally and a foe for cardiovascular homeostasis; on one hand providing protection against cellular injury, and on the other triggering damaging responses through innate and adaptive immunity. In this review we will discuss the functions of HSP60 and its effects on cells and the immune system regulation, only to later address its implications in the development and progression of CVD. Lastly, we summarize the outcome of various studies targeting HSP60 as a potential therapeutic strategy for cardiovascular and other diseases.
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