Evidence map›Paper›PMID 25542307›Full record

ArticleCellular signalling2015

Hyperglycemia enhances kidney cell injury in HIVAN through down-regulation of vitamin D receptors.

Partab Rai, Tejinder Singh, Rivka Lederman, Amrita Chawla, Dileep Kumar, Kang Cheng, Gautam Valecha, Peter W Mathieson, Moin A Saleem, Ashwani Malhotra and 1 more

Open access · greenAbstract read
In one paragraph

Article in Cellular signalling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

11 citing papers in PubMed, 20 citations in OpenAlex.

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  10. AT1R blockade in adverse milieus: role of SMRT and corepressor complexes.American journal of physiology. Renal physiology · 2015
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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

11 authors at 2 institutions in 2 countries.

Partab RaiDepartment of Medicine, Feinstein Institute for Medical Research, North Shore LIJ Medical School, NY, USA; Department of Pediatrics, University of Bristol, Bristol, UK.
Tejinder SinghDepartment of Medicine, Feinstein Institute for Medical Research, North Shore LIJ Medical School, NY, USA; Department of Pediatrics, University of Bristol, Bristol, UK.
Rivka LedermanDepartment of Medicine, Feinstein Institute for Medical Research, North Shore LIJ Medical School, NY, USA; Department of Pediatrics, University of Bristol, Bristol, UK.
Amrita ChawlaDepartment of Medicine, Feinstein Institute for Medical Research, North Shore LIJ Medical School, NY, USA; Department of Pediatrics, University of Bristol, Bristol, UK.
Dileep KumarDepartment of Medicine, Feinstein Institute for Medical Research, North Shore LIJ Medical School, NY, USA; Department of Pediatrics, University of Bristol, Bristol, UK.
Kang ChengDepartment of Medicine, Feinstein Institute for Medical Research, North Shore LIJ Medical School, NY, USA; Department of Pediatrics, University of Bristol, Bristol, UK.
Gautam ValechaDepartment of Medicine, Feinstein Institute for Medical Research, North Shore LIJ Medical School, NY, USA; Department of Pediatrics, University of Bristol, Bristol, UK.
Peter W MathiesonDepartment of Medicine, Feinstein Institute for Medical Research, North Shore LIJ Medical School, NY, USA; Department of Pediatrics, University of Bristol, Bristol, UK.
Moin A SaleemDepartment of Medicine, Feinstein Institute for Medical Research, North Shore LIJ Medical School, NY, USA; Department of Pediatrics, University of Bristol, Bristol, UK.
Ashwani MalhotraDepartment of Medicine, Feinstein Institute for Medical Research, North Shore LIJ Medical School, NY, USA; Department of Pediatrics, University of Bristol, Bristol, UK.
Pravin C SinghalDepartment of Medicine, Feinstein Institute for Medical Research, North Shore LIJ Medical School, NY, USA; Department of Pediatrics, University of Bristol, Bristol, UK. Electronic address: psinghal@nshs.edu.
University of Bristol · GBFeinstein Institute for Medical Research · US

Funding

p66ShcA in HIV associated NephropathyR01DK083931 · NIDDK · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI SINGHAL, PRAVIN C · 2010 to 2013
$2.5M
Epigenetic factors and HIV-associated NephropathyR01DK098074 · NIDDK · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI SINGHAL, PRAVIN C · 2013 to 2016
$2.5M
Renin Angioensin Aldosterone System in Drub Abuse and HIV-associated NephropathyR01DK084910 · NIDDK · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI SINGHAL, PRAVIN C · 2010 to 2014
$1.7M
NIDDK NIH HHS 1R01DK098074NIDDK NIH HHS R01 DK083931NIDDK NIH HHS R01 DK084910NIDDK NIH HHS R01DK084910NIDDK NIH HHS R01 DK098074
6 · The paper itself

Abstract

In the present study, we evaluated the effect of short term hyperglycemia on renal lesions in a mouse model (Tg26) of HIV-associated nephropathy (HIVAN). Control and Tg26 mice in groups (n=6) were administered either normal saline (FVBN or Tg) or streptozotocin (FVBN+STZ or Tg26+STZ). After two weeks, biomarkers were collected and kidneys were harvested. FVBN+ STZ and Tg26+STZ displayed elevated serum glucose levels when compared to FVBN and Tg26 respectively. Tg26+STZ displayed elevated (P<0.05) blood urea nitrogen (BUN) levels (P<0.05) and enhanced (P<0.01) proteinuria when compared to Tg26. Tg26+STZ displayed enhanced (P<0.001) number of sclerotic glomeruli and microcysts vs. Tg26. Renal tissues of Tg26 displayed down regulation of vitamin D receptor (VDR) expression and enhanced Ang II production when compared to FVBN mice. Hyperglycemia exacerbated down regulation of VDR and production of Ang II in FVBN and Tg mice. Hyperglycemia increased kidney cell reactive oxygen species (ROS) production and oxidative DNA damage in both FVBN and Tg26 mice. In in vitro studies, HIV down regulated podocyte VDR expression and also enhanced renin angiotensin system activation. In addition, both glucose and HIV stimulated kidney cell ROS generation and DNA damage and compromised DNA repair; however, tempol (superoxide dismutase mimetic), losartan (Ang II blocker) and EB1089 (VDR agonist) provided protection against DNA damaging effects of glucose and HIV. These findings indicated that glucose activated the RAS and inflicted oxidative stress-mediated DNA damage via down regulation of kidney cell VDR expression in HIV milieu both in vivo and in vitro.

Indexed as

AIDS-Associated NephropathyAngiotensinogenAnimalsCells, CulturedDown-Regulationgag Gene Products, Human Immunodeficiency VirusGlucoseHEK293 CellsHIV-1HumansHyperglycemiaKidney GlomerulusMiceMice, TransgenicPodocytespol Gene Products, Human Immunodeficiency VirusAngiotensinogengag Gene Products, Human Immunodeficiency VirusGlucosepol Gene Products, Human Immunodeficiency VirusReactive Oxygen SpeciesReceptors, CalcitriolStreptozocin8-OHdGDNA damageKidney injuryOxidative stress

Identifiers

PMID25542307
PMCPMC4347812
OpenAlexW2019472403

What OpenQuestion holds

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Registered trials

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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.