Evidence map›Paper›PMID 24386282›Full record

ArticlePloS one2013

Folic acid mitigates angiotensin-II-induced blood pressure and renal remodeling.

Sathnur B Pushpakumar, Sourav Kundu, Naira Metreveli, Utpal Sen

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
4.2field-weighted citation impact, top 7% 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

22 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
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  5. Observational
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  11. Frontiers in physiology · 2019
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  13. Hydrogen sulfide alleviates hypertensive kidney dysfunction through an epigenetic mechanism.American journal of physiology. Heart and circulatory physiology · 2017
    Article
  14. Article
  15. Article
  16. Review
  17. 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 1 institution in 1 country.

Sathnur B PushpakumarDepartment of Physiology and Biophysics, University of Louisville School of Medicine, Louisville, Kentucky, United States of America.
Sourav KunduDepartment of Physiology and Biophysics, University of Louisville School of Medicine, Louisville, Kentucky, United States of America.
Naira MetreveliDepartment of Physiology and Biophysics, University of Louisville School of Medicine, Louisville, Kentucky, United States of America.
Utpal SenDepartment of Physiology and Biophysics, University of Louisville School of Medicine, Louisville, Kentucky, United States of America.
University of Louisville · US

Funding

Homocysteine & Angiotensin II in Renovascular RemodelingR01HL104103 · NHLBI · UNIVERSITY OF LOUISVILLE · PI SEN, UTPAL · 2011 to 2015
$1.8M
NHLBI NIH HHS HL-104103NHLBI NIH HHS R01 HL104103
6 · The paper itself

Abstract

Clinical data suggests an association between systolic hypertension, renal function and hyperhomocysteinemia (HHcy). HHcy is a state of elevated plasma homocysteine (Hcy) levels and is known to cause vascular complications. In this study, we tested the hypothesis whether Ang II-induced hypertension increases plasma Hcy levels and contributes to renovascular remodeling. We also tested whether folic acid (FA) treatment reduces plasma Hcy levels by enhancing Hcy remethylation and thus mitigating renal remodeling. Hypertension was induced in WT mice by infusing Ang II using Alzet mini osmotic pumps. Blood pressure, Hcy level, renal vascular density, oxidative stress, inflammation and fibrosis markers, and angiogenic- and anti-angiogenic factors were measured. Ang II hypertension increased plasma Hcy levels and reduced renal cortical blood flow and microvascular density. Elevated Hcy in Ang II hypertension was associated with decreased 4, 5-Diaminofluorescein (DAF-2DA) staining suggesting impaired endothelial function. Increased expression of Nox-2, -4 and dihydroethidium stain revealed oxidative stress. Excess collagen IV deposition in the peri-glomerular area and increased MMP-2, and -9 expression and activity indicated renal remodeling. The mRNA and protein expression of asymmetric dimethylarginine (ADMA) was increased and eNOS protein was decreased suggesting the involvement of this pathway in Hcy mediated hypertension. Decreased expressions of VEGF and increased anti-angiogenic factors, angiostatin and endostatin indicated impaired vasculogenesis. FA treatment partially reduced hypertension by mitigating HHcy in Ang II-treated animals and alleviated pro-inflammatory, pro-fibrotic and anti-angiogenic factors. These results suggest that renovascular remodeling in Ang II-induced hypertension is, in part, due to HHcy.

Indexed as

Angiotensin IIAnimalsArginineBlood PressureCollagenDrinkingFolic AcidGene Expression Regulation, EnzymologicHomocysteineHyperhomocysteinemiaHypertensionKidneyMatrix MetalloproteinasesMiceMice, Inbred C57BLNitric OxideAngiotensin IIArginineCollagendimethylarginineFolic AcidHomocysteineMatrix MetalloproteinasesNitric OxideNitric Oxide Synthase Type IIIRNA, MessengerTissue Inhibitor of Metalloproteinases

Identifiers

PMID24386282
PMCPMC3873386
OpenAlexW2039291409

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.