Evidence map›Paper›PMID 34356879›Full record

ArticleBiomedicines2021

Delayed Contralateral Nephrectomy Halted Post-Ischemic Renal Fibrosis Progression and Inhibited the Ischemia-Induced Fibromir Upregulation in Mice.

Beáta Róka, Pál Tod, Tamás Kaucsár, Éva Nóra Bukosza, Imre Vörös, Zoltán V Varga, Balázs Petrovich, Bence Ágg, Péter Ferdinandy, Gábor Szénási and 1 more

Open access · goldAbstract read
In one paragraph

Article in Biomedicines, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.4field-weighted citation impact, top 46% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
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 1 institution in 1 country.

Beáta RókaInstitute of Translational Medicine, Semmelweis University, 1094 Budapest, Hungary.
Pál TodInstitute of Translational Medicine, Semmelweis University, 1094 Budapest, Hungary.
Tamás KaucsárInstitute of Translational Medicine, Semmelweis University, 1094 Budapest, Hungary.
Éva Nóra BukoszaInstitute of Translational Medicine, Semmelweis University, 1094 Budapest, Hungary.ORCID 0000-0001-7606-7824
Imre VörösDepartment of Pharmacology and Pharmacotherapy, Semmelweis University, 1089 Budapest, Hungary.ORCID 0000-0001-5922-6109
Zoltán V VargaDepartment of Pharmacology and Pharmacotherapy, Semmelweis University, 1089 Budapest, Hungary.
Balázs PetrovichDepartment of Pharmacology and Pharmacotherapy, Semmelweis University, 1089 Budapest, Hungary.
Bence ÁggDepartment of Pharmacology and Pharmacotherapy, Semmelweis University, 1089 Budapest, Hungary.ORCID 0000-0002-6492-0426
Péter FerdinandyDepartment of Pharmacology and Pharmacotherapy, Semmelweis University, 1089 Budapest, Hungary.
Gábor SzénásiInstitute of Translational Medicine, Semmelweis University, 1094 Budapest, Hungary.ORCID 0000-0002-7350-6091
Péter HamarInstitute of Translational Medicine, Semmelweis University, 1094 Budapest, Hungary.ORCID 0000-0002-1095-3564
Semmelweis University · HU

Funding

European Union's Horizon 2020 research and innovation programme 739593Hungarian Academy of Sciences János Bolyai Research ScholarshipHungarian Research Fund ANN-110810Hungarian Research Fund OTKA FK-134751Hungarian Research Fund OTKA SNN-114619National Research, Development and Innovation Fund of Hungary EFOP-3.6.3-VEKOP-16-2017-00009National Research, Development and Innovation Fund of Hungary NVKP_16-1-2016-0042National Research, Development and Innovation Office of Hungary NVKP-16-1-2016-0017 National Heart ProgramNational Research, Development and Innovation Office of the Ministry of Innovation and Technology in Hungary TKP/ITM/NKFIH Research Excellence ProgrammeSemmelweis University Therapeutic Development thematic programmeUniversity of Pécs Kispál Gyula startup grant (300021)
6 · The paper itself

Abstract

(1) Background: Ischemia reperfusion (IR) is the leading cause of acute kidney injury (AKI) and results in predisposition to chronic kidney disease. We demonstrated that delayed contralateral nephrectomy (Nx) greatly improved the function of the IR-injured kidney and decelerated fibrosis progression. Our aim was to identify microRNAs (miRNA/miR) involved in this process. (2) Methods: NMRI mice were subjected to 30 min of renal IR and one week later to Nx/sham surgery. The experiments were conducted for 7-28 days after IR. On day 8, multiplex renal miRNA profiling was performed. Expression of nine miRNAs was determined with qPCR at all time points. Based on the target prediction, plexin-A2 and Cd2AP were measured by Western blot. (3) Results: On day 8 after IR, the expression of 20/1195 miRNAs doubled, and 9/13 selected miRNAs were upregulated at all time points. Nx reduced the expression of several ischemia-induced pro-fibrotic miRNAs (fibromirs), such as miR-142a-duplex, miR-146a-5p, miR-199a-duplex, miR-214-3p and miR-223-3p, in the injured kidneys at various time points. Plexin-A2 was upregulated by IR on day 10, while Cd2AP was unchanged. (4) Conclusion: Nx delayed fibrosis progression and decreased the expression of ischemia-induced fibromirs. The protein expression of plexin-A2 and Cd2AP is mainly regulated by factors other than miRNAs.

Indexed as

ischemia-reperfusion injurykidney fibrosismicemicroRNAs

Identifiers

PMID34356879
PMCPMC8301422
OpenAlexW3181736695

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.