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Published on: May 22, 2014
Relationship between hyperuricemia, HSP70 and NLRP3 inflammasome in arterial hypertension
Bernardo Rodríguez-Iturbe1,2, Richard J Johnson3, Laura G Sánchez-Lozada4
1Department of Nephrology and Mineral Metabolism, INCMN Salvador Zubirán, Mexico City, Mexico.
Insights
Inflammation and autoimmune responses contribute to primary hypertension. This review explores how hyperuricemia and heat shock protein 70 (HSP70) activate the inflammasome, a key factor in hypertension development.
Area of Science:
- Cardiovascular Research
- Immunology
- Nephrology
Background:
- Arterial hypertension is a leading global cardiovascular risk factor, causing millions of deaths annually.
- Primary hypertension, lacking a clear cause, affects a significant portion of the population.
- Inflammation and autoimmune responses are implicated in the sodium retention and hemodynamic changes driving primary hypertension.
Approach:
- Review of experimental and clinical investigations on inflammation in primary hypertension.
- Focus on the roles of hyperuricemia and heat shock proteins (HSP), specifically HSP70.
- Examination of the interrelation between hyperuricemia, extracellular HSP70, and inflammasome activation.
Key Points:
- Hyperuricemia and HSP70 are linked to innate immunity activation and inflammatory responses in hypertension.
- Clinical studies show associations between HSP70 expression, anti-HSP70 antibodies, and primary hypertension.
- The inflammasome is a potential central player in the pathophysiology of primary hypertension.
Conclusions:
- Inflammation and autoimmune reactivity are critical components of primary hypertension.
- Hyperuricemia and extracellular HSP70 may drive hypertension through inflammasome activation.
- Further research into these pathways could reveal novel therapeutic targets for hypertension.
Abstract:
Arterial hypertension is the most important cardiovascular risk factor in chronic non-communicable diseases and is estimated to be responsible for 10.4 million deaths annually. The global prevalence of hypertension is 30% and the majority of people with hypertension do not have a clear identifiable cause and are considered to have primary hypertension. Experimental and clinical investigations from several research groups, including ours, have established that inflammation and autoimmune reactivity play a role in the sodium retention and hemodynamic responses that drive primary hypertension. Hyperuricemia and heat stress proteins (HSP), particularly HSP70, are both associated with the activation of innate immunity that plays a role in the development of inflammatory reactivity in the hypertensive patient. Clinical studies have shown an association between the expression of HSP70 and anti-HSP70 antibodies and primary hypertension. This brief review aims to examine the interrelation between hyperuricemia and extracellular overexpression of HSP70 in the activation of the inflammasome that may have a central role in the pathophysiology of primary hypertension.
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