Evidence map›Paper›PMID 27927651›Full record

ReviewAmerican journal of physiology. Renal physiology2017

DNA repair in ischemic acute kidney injury.

Jeffrey D Pressly, Frank Park

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of physiology. Renal physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

20 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  13. Emerging role of tumor suppressor p53 in acute and chronic kidney diseases.Cellular and molecular life sciences : CMLS · 2022
    Review
  14. NADSignal transduction and targeted therapy · 2020
    Review
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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

2 authors at 1 institution in 1 country.

Jeffrey D PresslyDepartment of Pharmaceutical Sciences, College of Pharmacy, University of Tennessee Health Science Center, Memphis, Tennessee jpressly@uthsc.edu.
Frank ParkDepartment of Pharmaceutical Sciences, College of Pharmacy, University of Tennessee Health Science Center, Memphis, Tennessee.
University of Tennessee Health Science Center · US

Funding

AGS3 in Ischemic Renal InjuryR01DK090123 · NIDDK · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI PARK, FRANK, REGNER, KEVIN R. · 2011 to 2015
$1.5M
6 · The paper itself

Abstract

Ischemia-reperfusion injury (IRI) is a common cause of acute kidney injury leading to an induction of oxidative stress, cellular dysfunction, and loss of renal function. DNA damage, including oxidative base modifications and physical DNA strand breaks, is a consequence of renal IRI. Like many other organs in the body, a redundant and highly conserved set of endogenous repair pathways have evolved to selectively recognize the various types of cellular DNA damage and combat its negative effects on cell viability. Severe damage to the DNA, however, can trigger cell death and elimination of the injured tubular epithelial cells. In this minireview, we summarize the state of the current field of DNA damage and repair in the kidney and provide some expected and, in some cases, unexpected effects of IRI on DNA damage and repair in the kidney. These findings may be applicable to other forms of acute kidney injury and could provide new opportunities for renal research.

Indexed as

DNA DamageDNA RepairAcute Kidney InjuryAnimalsCell DeathCell ProliferationEpithelial CellsHumansKidney TubulesOxidative StressReperfusion InjurySignal Transductionacute kidney injuryDNA repairTRIP13tubular epithelial cells

Identifiers

PMID27927651
PMCPMC5407066
OpenAlexW2560132062

What OpenQuestion holds

Textmetadata
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.