Evidence map›Paper›PMID 24516656›Full record

ArticlePloS one2014

Id proteins regulate capillary repair and perivascular cell proliferation following ischemia-reperfusion injury.

David Lee, Shantheri Shenoy, Yezina Nigatu, Matt Plotkin

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-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

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. The role of Id genes on pulmonary hypertension development in left heart failure.American heart journal plus : cardiology research and practice · 2026
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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.

David LeeDepartment of Medicine, Renal Research Division, New York Medical College, Valhalla, New York, United States of America.
Shantheri ShenoyDepartment of Medicine, Renal Research Division, New York Medical College, Valhalla, New York, United States of America.
Yezina NigatuDepartment of Medicine, Renal Research Division, New York Medical College, Valhalla, New York, United States of America.
Matt PlotkinDepartment of Medicine, Renal Research Division, New York Medical College, Valhalla, New York, United States of America.
New York Medical College · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute kidney injury (AKI) results in microvascular damage that if not normally repaired, may lead to fibrosis. The Id1 and 3 proteins have a critical role in promoting angiogenesis during development, tumor growth and wound repair by functioning as dominant negative regulators of bHLH transcription factors. The goal of this study was to determine if Id proteins regulate microvascular repair and remodeling and if increased Id1 expression results in decreased capillary loss following AKI. The effect of changes in Id expression in vivo was examined using Id1-/-, Id3RFP/+ (Id1/Id3 KO) and Tek (Tie2)-rtTA, TRE-lacz/TRE Id1 (TRE Id1) mice with doxycycline inducible endothelial Id1 and β-galactosidase expression. Id1 and 3 were co-localized in endothelial cells in normal adult kidneys and protein levels were increased at day 3 following ischemia-reperfusion injury (IRI) and contralateral nephrectomy. Id1/Id3 KO mice had decreased baseline capillary density and pericyte coverage and increased tubular damage following IRI but decreased interstitial cell proliferation and fibrosis compared with WT littermates. No compensatory increase in kidney size occurred in KO mice resulting in increased creatinine compared with WT and TRE Id1 mice. TRE Id1 mice had no capillary rarefaction within 1 week following IRI in comparison with WT littermates. TRE Id1 mice had increased proliferation of PDGFRβ positive interstitial cells and medullary collagen deposition and developed capillary rarefaction and albuminuria at later time points. These differences were associated with increased Angiopoietin 1 (Ang1) and decreased Ang2 expression in TRE Id1 mice. Examination of gene expression in microvascular cells isolated from WT, Id1/Id3 KO and TRE Id1 mice showed increased Ang1 and αSMA in Id1 overexpressing cells and decreased pericyte markers in cells from KO mice. These results suggest that increased Id levels following AKI result in microvascular remodeling associated with increased fibrosis.

Indexed as

Acute Kidney InjuryAnimalsCapillariesCell ProliferationFibrosisInhibitor of Differentiation Protein 1Inhibitor of Differentiation ProteinsKidneyMaleMiceMice, KnockoutOrgan SizePericytesReperfusion InjuryIdb1 protein, mouseIdb3 protein, mouseInhibitor of Differentiation Protein 1Inhibitor of Differentiation Proteins

Identifiers

PMID24516656
PMCPMC3917915
OpenAlexW2091581420

What OpenQuestion holds

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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.