HSP70 and Primary Arterial Hypertension
Heat shock protein 70 (HSP70) production is a stress-generated cellular response with high interspecies homology. HSP70 has both chaperone and cytokine functions and may induce, depending on the context, tolerogenic anti-inflammatory reactivity or immunogenic and autoimmune reactivity. Intracellular...
Main Authors: | , , , |
---|---|
Format: | Article |
Language: | English |
Published: |
MDPI AG
2023-02-01
|
Series: | Biomolecules |
Subjects: | |
Online Access: | https://www.mdpi.com/2218-273X/13/2/272 |
_version_ | 1827758329117540352 |
---|---|
author | Bernardo Rodriguez-Iturbe Richard J. Johnson Laura Gabriela Sanchez-Lozada Hector Pons |
author_facet | Bernardo Rodriguez-Iturbe Richard J. Johnson Laura Gabriela Sanchez-Lozada Hector Pons |
author_sort | Bernardo Rodriguez-Iturbe |
collection | DOAJ |
description | Heat shock protein 70 (HSP70) production is a stress-generated cellular response with high interspecies homology. HSP70 has both chaperone and cytokine functions and may induce, depending on the context, tolerogenic anti-inflammatory reactivity or immunogenic and autoimmune reactivity. Intracellular (chaperoning transit of antigens to MHC in antigen-presenting cells) and extracellular HSP70-related effects are associated with hypertension, which is an inflammatory condition recognized as the most important risk factor for cardiovascular disease mortality. Here, we review (a) the relationship between HSP70, inflammation and immune reactivity, (b) clinical evidence relating to stress, HSP70 and anti-HSP70 reactivity with primary hypertension and (c) experimental data showing that salt-sensitive hypertension is associated with delayed hypersensitivity to HSP70. This is a consequence of anti-HSP70 reactivity in the kidneys and may be prevented and corrected by the T-cell-driven inhibition of kidney inflammation triggered by specific epitopes of HSP70. Finally, we discuss our postulate that lifelong stress signals and danger-associated molecular patterns stimulate HSP-70 and individual genetic and epigenetic characteristics determine whether the HSP70 response would drive inflammatory immune reactivity causing hypertension or, alternatively, would drive immunomodulatory responses that protect against hypertension. |
first_indexed | 2024-03-11T09:06:09Z |
format | Article |
id | doaj.art-9c76f1b791124c2a9dc7c472de00e71a |
institution | Directory Open Access Journal |
issn | 2218-273X |
language | English |
last_indexed | 2024-03-11T09:06:09Z |
publishDate | 2023-02-01 |
publisher | MDPI AG |
record_format | Article |
series | Biomolecules |
spelling | doaj.art-9c76f1b791124c2a9dc7c472de00e71a2023-11-16T19:22:49ZengMDPI AGBiomolecules2218-273X2023-02-0113227210.3390/biom13020272HSP70 and Primary Arterial HypertensionBernardo Rodriguez-Iturbe0Richard J. Johnson1Laura Gabriela Sanchez-Lozada2Hector Pons3Department of Nephrology, Instituto Nacional de Ciencias Médicas y Nutrición “Salvador Zubirán”, Mexico City 14080, MexicoDivision of Renal Diseases and Hypertension, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USADepartment of Cardio-Renal Physiopathology, National Institute of Cardiology Ignacio Chávez, Mexico City 14080, MexicoFacultad de Medicina, Universidad del Zulia, Maracaibo 4011, VenezuelaHeat shock protein 70 (HSP70) production is a stress-generated cellular response with high interspecies homology. HSP70 has both chaperone and cytokine functions and may induce, depending on the context, tolerogenic anti-inflammatory reactivity or immunogenic and autoimmune reactivity. Intracellular (chaperoning transit of antigens to MHC in antigen-presenting cells) and extracellular HSP70-related effects are associated with hypertension, which is an inflammatory condition recognized as the most important risk factor for cardiovascular disease mortality. Here, we review (a) the relationship between HSP70, inflammation and immune reactivity, (b) clinical evidence relating to stress, HSP70 and anti-HSP70 reactivity with primary hypertension and (c) experimental data showing that salt-sensitive hypertension is associated with delayed hypersensitivity to HSP70. This is a consequence of anti-HSP70 reactivity in the kidneys and may be prevented and corrected by the T-cell-driven inhibition of kidney inflammation triggered by specific epitopes of HSP70. Finally, we discuss our postulate that lifelong stress signals and danger-associated molecular patterns stimulate HSP-70 and individual genetic and epigenetic characteristics determine whether the HSP70 response would drive inflammatory immune reactivity causing hypertension or, alternatively, would drive immunomodulatory responses that protect against hypertension.https://www.mdpi.com/2218-273X/13/2/272HSP70hypertensionimmune reactivityinflammation |
spellingShingle | Bernardo Rodriguez-Iturbe Richard J. Johnson Laura Gabriela Sanchez-Lozada Hector Pons HSP70 and Primary Arterial Hypertension Biomolecules HSP70 hypertension immune reactivity inflammation |
title | HSP70 and Primary Arterial Hypertension |
title_full | HSP70 and Primary Arterial Hypertension |
title_fullStr | HSP70 and Primary Arterial Hypertension |
title_full_unstemmed | HSP70 and Primary Arterial Hypertension |
title_short | HSP70 and Primary Arterial Hypertension |
title_sort | hsp70 and primary arterial hypertension |
topic | HSP70 hypertension immune reactivity inflammation |
url | https://www.mdpi.com/2218-273X/13/2/272 |
work_keys_str_mv | AT bernardorodrigueziturbe hsp70andprimaryarterialhypertension AT richardjjohnson hsp70andprimaryarterialhypertension AT lauragabrielasanchezlozada hsp70andprimaryarterialhypertension AT hectorpons hsp70andprimaryarterialhypertension |