Evidence map›Paper›PMID 28774305›Full record

ArticleBMC endocrine disorders2017

Renal injury is accelerated by global hypoxia-inducible factor 1 alpha deficiency in a mouse model of STZ-induced diabetes.

Romana Bohuslavova, Radka Cerychova, Katerina Nepomucka, Gabriela Pavlinkova

Open access · goldAbstract read
In one paragraph

Article in BMC endocrine disorders, 2017. 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
1.1field-weighted citation impact, top 26% 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, 31 citations in OpenAlex.

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  9. Susceptibility of renal fibrosis in diabetes: Role of hypoxia inducible factor-1.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
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  12. Network Pharmacology-Based Prediction of Mechanism of Shenzhuo Formula for Application to DKD.Evidence-based complementary and alternative medicine : eCAM · 2021
    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.

Romana BohuslavovaLaboratory of Molecular Pathogenetics, Institute of Biotechnology CAS, BIOCEV, Center of Excellence, Prumyslova 595, Vestec, 25242, Czechia.
Radka CerychovaLaboratory of Molecular Pathogenetics, Institute of Biotechnology CAS, BIOCEV, Center of Excellence, Prumyslova 595, Vestec, 25242, Czechia.
Katerina NepomuckaLaboratory of Molecular Pathogenetics, Institute of Biotechnology CAS, BIOCEV, Center of Excellence, Prumyslova 595, Vestec, 25242, Czechia.
Gabriela PavlinkovaLaboratory of Molecular Pathogenetics, Institute of Biotechnology CAS, BIOCEV, Center of Excellence, Prumyslova 595, Vestec, 25242, Czechia. gpavlinkova@ibt.cas.cz.
Czech Academy of Sciences, Institute of Biotechnology · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHypoxia inducible factor 1 (HIF-1) activates protective pathways to counteract hypoxia and prevent tissue damage in conjunction with renal injury. The aim of this study was to evaluate a role of HIF-1 in diabetes-induced kidney damage.

methodsWe used a streptozotocin-induced diabetes mouse model and compared biochemical, histological and molecular parameters associated with kidney damage in Hif1α deficient (Hif1α

resultsWe showed that Hif1α deficiency accelerated pathological changes in the early stage of DN. Six weeks after diabetes-induction, Hif1α deficient mice showed more prominent changes in biochemical serum parameters associated with glomerular injury, increased expression of podocyte damage markers, and loss of podocytes compared to wild-type mice. These results indicate that Hif1α deficiency specifically affects podocyte survival in the early phase of DN, resulting in diabetic glomerular injury. In contrast, renal fibrosis was not affected by the global reduction of Hif1α, at least not in the early phase of diabetic exposure.

conclusionsTogether our data reveal that HIF-1 has an essential role in the early response to prevent diabetes-induced tissue damage and that impaired HIF-1 signaling results in a faster progression of DN. Although the modulation of HIF-1 activity is a high-priority target for clinical treatments, further study is required to investigate HIF-1 as a potential therapeutic target for the treatment of DN.

Indexed as

Disease Models, AnimalAnimalsDiabetes Mellitus, ExperimentalDiabetic NephropathiesHypoxia-Inducible Factor 1, alpha SubunitMaleMicePrognosisHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitDiabetic complicationsDiabetic nephropathyHypoxiaMouse modelPodocyte

Identifiers

PMID28774305
PMCPMC5543752
OpenAlexW2744937310

What OpenQuestion holds

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LicenceCC BY
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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.