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The role of autoimmune reactivity induced by heat shock protein 70 in the pathogenesis of essential hypertension
Author(s) -
RodriguezIturbe Bernardo,
Lanaspa Miguel A,
Johnson Richard J
Publication year - 2019
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/bph.14334
Subject(s) - autoimmunity , heat shock protein , molecular mimicry , pathogenesis , immunology , hsp70 , immune system , inflammation , essential hypertension , acquired immune system , biology , immunity , medicine , endocrinology , genetics , blood pressure , gene
Autoimmunity is increasingly recognized as having a central role in essential hypertension. Heat shock proteins (HSPs) are immunodominant molecules with high interspecies homology and autoimmune reactivity directed against HSP70 may play a role in the pathogenesis of hypertension. Autoimmunity to HSP70 may result from molecular mimicry between human HSP and bacterial HSP or, alternatively, as a response to HSP70–peptide complexes generated during cellular stress and delivered to the major histocompatibility complex by antigen‐presenting cells. HSP70 is increased in the circulation and kidney of hypertensive patients, and genetic polymorphisms of HSP70 are associated with essential hypertension. Depending on the route and conditions of administration, HSP70 may induce or suppress immune‐related inflammation. Renal inflammation induced by immunity to HSP70 causes hypertension in laboratory animals, and administration of specific peptide sequences of HSP70 results in a protective anti‐inflammatory response that prevents and corrects salt‐induced hypertension. Potential therapeutic uses of HSP70 in essential hypertension deserve to be investigated. Linked Articles This article is part of a themed section on Immune Targets in Hypertension. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.12/issuetoc