Evidence map›Paper›PMID 22664958›Full record

ArticleDiabetes2012

Heterogeneous nuclear ribonucleoprotein F suppresses angiotensinogen gene expression and attenuates hypertension and kidney injury in diabetic mice.

Chao-Sheng Lo, Shiao-Ying Chang, Isabelle Chenier, Janos G Filep, Julie R Ingelfinger, Shao Ling Zhang, John S D Chan

Open access · hybridAbstract read
In one paragraph

Article in Diabetes, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

25 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
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  16. Review
  17. Src family kinases in chronic kidney disease.American journal of physiology. Renal physiology · 2017
    Review
  18. Article
  19. Article
  20. Diabetes Induces Aberrant DNA Methylation in the Proximal Tubules of the Kidney.Journal of the American Society of Nephrology : JASN · 2015
    Article
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

7 authors at 4 institutions in 2 countries.

Chao-Sheng LoCentre de Recherche du Centre Hospitalier de l'Université de Montréal, Université de Montréal, Hôtel-Dieu Hospital, Montreal, Quebec, Canada.
Shiao-Ying Chang
Isabelle Chenier
Janos G Filep
Julie R Ingelfinger
Shao Ling Zhang
John S D Chan
Hotel Dieu Hospital · CACentre Hospitalier de l’Université de Montréal · CAHôpital Maisonneuve-Rosemont · CAMassachusetts General Hospital · US

Funding

ROLES OF THE PROXIMAL TUBULE RENIN ANGIOTENSIN SYSTEMR01HL048455 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI INGELFINGER, JULIE R. · 1992 to 2000
$295k
Canadian Institutes of Health Research MOP-16088Canadian Institutes of Health Research MOP-64283Canadian Institutes of Health Research MOP-84363Canadian Institutes of Health Research MOP-86450Canadian Institutes of Health Research MOP-93650NHLBI NIH HHS HL-48455
6 · The paper itself

Abstract

We investigated the impact of heterogeneous nuclear ribonucleoprotein F (hnRNP F) overexpression on angiotensinogen (Agt) gene expression, hypertension, and renal proximal tubular cell (RPTC) injury in high-glucose milieu both in vivo and in vitro. Diabetic Akita transgenic (Tg) mice specifically overexpressing hnRNP F in their RPTCs were created, and the effects on systemic hypertension, Agt gene expression, renal hypertrophy, and interstitial fibrosis were studied. We also examined immortalized rat RPTCs stably transfected with control plasmid or plasmid containing hnRNP F cDNA in vitro. The results showed that hnRNP F overexpression attenuated systemic hypertension, suppressed Agt and transforming growth factor-β1 (TGF-β1) gene expression, and reduced urinary Agt and angiotensin II levels, renal hypertrophy, and glomerulotubular fibrosis in Akita hnRNP F-Tg mice. In vitro, hnRNP F overexpression prevented the high-glucose stimulation of Agt and TGF-β1 mRNA expression and cellular hypertrophy in RPTCs. These data suggest that hnRNP F plays a modulatory role and can ameliorate hypertension, renal hypertrophy, and interstitial fibrosis in diabetes. The underlying mechanism is mediated, at least in part, via the suppression of intrarenal Agt gene expression in vivo. hnRNP F may be a potential target in the treatment of hypertension and kidney injury in diabetes.

Indexed as

AngiotensinogenAnimalsDiabetes Mellitus, ExperimentalDiabetic NephropathiesFibrosisGene ExpressionHeterogeneous-Nuclear Ribonucleoprotein Group F-HHypertensionKidneyKidney DiseasesMiceMice, TransgenicRenin-Angiotensin SystemTransforming Growth Factor beta1AngiotensinogenHeterogeneous-Nuclear Ribonucleoprotein Group F-HTransforming Growth Factor beta1

Identifiers

PMID22664958
PMCPMC3447919
OpenAlexW2160163608

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.