Molecular Mechanisms of Hypertensive Nephropathy: Renoprotective Effect of Losartan through Hsp70

Hypertensive nephrosclerosis is the second most common cause of end-stage renal disease after diabetes. For years, hypertensive kidney disease has been focused on the afferent arterioles and glomeruli damage and the involvement of the renin angiotensin system (RAS). Nonetheless, in recent years, nov...

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Autores principales: Valeria Victoria Costantino, Andrea Fernanda Gil Lorenzo, Victoria Bocanegra, Patricia G. Vallés
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Publicado: MDPI AG 2021
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spelling oai:doaj.org-article:977416c478684c7f947e7b2f417af5692021-11-25T17:11:57ZMolecular Mechanisms of Hypertensive Nephropathy: Renoprotective Effect of Losartan through Hsp7010.3390/cells101131462073-4409https://doaj.org/article/977416c478684c7f947e7b2f417af5692021-11-01T00:00:00Zhttps://www.mdpi.com/2073-4409/10/11/3146https://doaj.org/toc/2073-4409Hypertensive nephrosclerosis is the second most common cause of end-stage renal disease after diabetes. For years, hypertensive kidney disease has been focused on the afferent arterioles and glomeruli damage and the involvement of the renin angiotensin system (RAS). Nonetheless, in recent years, novel evidence has demonstrated that persistent high blood pressure injures tubular cells, leading to epithelial–mesenchymal transition (EMT) and tubulointerstitial fibrosis. Injury primarily determined at the glomerular level by hypertension causes changes in post-glomerular peritubular capillaries that in turn induce endothelial damage and hypoxia. Microvasculature dysfunction, by inducing hypoxic environment, triggers inflammation, EMT with epithelial cells dedifferentiation and fibrosis. Hypertensive kidney disease also includes podocyte effacement and loss, leading to disruption of the filtration barrier. This review highlights the molecular mechanisms and histologic aspects involved in the pathophysiology of hypertensive kidney disease incorporating knowledge about EMT and tubulointerstitial fibrosis. The role of the Hsp70 chaperone on the angiotensin II–induced EMT after angiotensin II type 1 receptor (AT<sub>1</sub>R) blockage, as a possible molecular target for therapeutic strategy against hypertensive renal damage is discussed.Valeria Victoria CostantinoAndrea Fernanda Gil LorenzoVictoria BocanegraPatricia G. VallésMDPI AGarticlehypertensionnephrosclerosisepithelial–mesenchymal transitionHsp70 chaperoneproximal tubule epithelial cellsBiology (General)QH301-705.5ENCells, Vol 10, Iss 3146, p 3146 (2021)
institution DOAJ
collection DOAJ
language EN
topic hypertension
nephrosclerosis
epithelial–mesenchymal transition
Hsp70 chaperone
proximal tubule epithelial cells
Biology (General)
QH301-705.5
spellingShingle hypertension
nephrosclerosis
epithelial–mesenchymal transition
Hsp70 chaperone
proximal tubule epithelial cells
Biology (General)
QH301-705.5
Valeria Victoria Costantino
Andrea Fernanda Gil Lorenzo
Victoria Bocanegra
Patricia G. Vallés
Molecular Mechanisms of Hypertensive Nephropathy: Renoprotective Effect of Losartan through Hsp70
description Hypertensive nephrosclerosis is the second most common cause of end-stage renal disease after diabetes. For years, hypertensive kidney disease has been focused on the afferent arterioles and glomeruli damage and the involvement of the renin angiotensin system (RAS). Nonetheless, in recent years, novel evidence has demonstrated that persistent high blood pressure injures tubular cells, leading to epithelial–mesenchymal transition (EMT) and tubulointerstitial fibrosis. Injury primarily determined at the glomerular level by hypertension causes changes in post-glomerular peritubular capillaries that in turn induce endothelial damage and hypoxia. Microvasculature dysfunction, by inducing hypoxic environment, triggers inflammation, EMT with epithelial cells dedifferentiation and fibrosis. Hypertensive kidney disease also includes podocyte effacement and loss, leading to disruption of the filtration barrier. This review highlights the molecular mechanisms and histologic aspects involved in the pathophysiology of hypertensive kidney disease incorporating knowledge about EMT and tubulointerstitial fibrosis. The role of the Hsp70 chaperone on the angiotensin II–induced EMT after angiotensin II type 1 receptor (AT<sub>1</sub>R) blockage, as a possible molecular target for therapeutic strategy against hypertensive renal damage is discussed.
format article
author Valeria Victoria Costantino
Andrea Fernanda Gil Lorenzo
Victoria Bocanegra
Patricia G. Vallés
author_facet Valeria Victoria Costantino
Andrea Fernanda Gil Lorenzo
Victoria Bocanegra
Patricia G. Vallés
author_sort Valeria Victoria Costantino
title Molecular Mechanisms of Hypertensive Nephropathy: Renoprotective Effect of Losartan through Hsp70
title_short Molecular Mechanisms of Hypertensive Nephropathy: Renoprotective Effect of Losartan through Hsp70
title_full Molecular Mechanisms of Hypertensive Nephropathy: Renoprotective Effect of Losartan through Hsp70
title_fullStr Molecular Mechanisms of Hypertensive Nephropathy: Renoprotective Effect of Losartan through Hsp70
title_full_unstemmed Molecular Mechanisms of Hypertensive Nephropathy: Renoprotective Effect of Losartan through Hsp70
title_sort molecular mechanisms of hypertensive nephropathy: renoprotective effect of losartan through hsp70
publisher MDPI AG
publishDate 2021
url https://doaj.org/article/977416c478684c7f947e7b2f417af569
work_keys_str_mv AT valeriavictoriacostantino molecularmechanismsofhypertensivenephropathyrenoprotectiveeffectoflosartanthroughhsp70
AT andreafernandagillorenzo molecularmechanismsofhypertensivenephropathyrenoprotectiveeffectoflosartanthroughhsp70
AT victoriabocanegra molecularmechanismsofhypertensivenephropathyrenoprotectiveeffectoflosartanthroughhsp70
AT patriciagvalles molecularmechanismsofhypertensivenephropathyrenoprotectiveeffectoflosartanthroughhsp70
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