Evidence map›Paper›PMID 34831368›Full record

ReviewCells2021

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

Valeria Victoria Costantino, Andrea Fernanda Gil Lorenzo, Victoria Bocanegra, Patricia G Vallés

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 1 pooled it
8.2field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

55 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.

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  19. [Mechanism of Trifolin in Attenuating Hypertension-Induced Renal Cell Apoptosis via Modulation of the MAPK Signaling Pathway].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2025
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Valeria Victoria CostantinoIMBECU-CONICET, Instituto de Medicina y Biología Experimental de Cuyo-Consejo Nacional de Investigaciones Científicas y Técnicas, Mendoza 5500, Argentina.ORCID 0000-0002-3707-8843
Andrea Fernanda Gil LorenzoÁrea de Fisiopatología, Departamento de Patología, Facultad de Ciencias Médicas, Universidad Nacional de Cuyo, Mendoza 5500, Argentina.
Victoria BocanegraIMBECU-CONICET, Instituto de Medicina y Biología Experimental de Cuyo-Consejo Nacional de Investigaciones Científicas y Técnicas, Mendoza 5500, Argentina.
Patricia G VallésIMBECU-CONICET, Instituto de Medicina y Biología Experimental de Cuyo-Consejo Nacional de Investigaciones Científicas y Técnicas, Mendoza 5500, Argentina.
Consejo Nacional de Investigaciones Científicas y Técnicas · ARUniversidad Nacional de Cuyo · AR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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

Indexed as

AnimalsEpithelial-Mesenchymal TransitionHSP70 Heat-Shock ProteinsHumansHypertension, RenalKidneyLosartanNephritisProtective AgentsHSP70 Heat-Shock ProteinsLosartanProtective Agentsepithelial–mesenchymal transitionHsp70 chaperonehypertensionnephrosclerosisproximal tubule epithelial cells

Identifiers

PMID34831368
PMCPMC8619557
OpenAlexW3211526443

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.