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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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) |
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hypertension nephrosclerosis epithelial–mesenchymal transition Hsp70 chaperone proximal tubule epithelial cells Biology (General) QH301-705.5 |
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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 |
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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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1718412667067039744 |