Evidence map›Paper›PMID 28935640›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2018

Attenuation of pulmonary ACE2 activity impairs inactivation of des-Arg

Chhinder P Sodhi, Christine Wohlford-Lenane, Yukihiro Yamaguchi, Thomas Prindle, William B Fulton, Sanxia Wang, Paul B McCray, Mark Chappell, David J Hackam, Hongpeng Jia

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PubMed Full text at PMC Publisher
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 234 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
234citing papers in PubMed, 2 pooled it
23.9field-weighted citation impact, top 1% 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

234 citing papers in PubMed, 2 syntheses or guidelines pooled it, 351 citations in OpenAlex.

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174 more citing papers are in PubMed but not listed here.

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

10 authors at 3 institutions in 1 country.

Chhinder P SodhiDivision of Pediatric Surgery, Department of Surgery, Johns Hopkins University , Baltimore, Maryland.
Christine Wohlford-LenaneDepartment of Pediatrics, Carver College of Medicine, The University of Iowa , Iowa City, Iowa.
Yukihiro YamaguchiDivision of Pediatric Surgery, Department of Surgery, Johns Hopkins University , Baltimore, Maryland.
Thomas PrindleDivision of Pediatric Surgery, Department of Surgery, Johns Hopkins University , Baltimore, Maryland.
William B FultonDivision of Pediatric Surgery, Department of Surgery, Johns Hopkins University , Baltimore, Maryland.
Sanxia WangDivision of Pediatric Surgery, Department of Surgery, Johns Hopkins University , Baltimore, Maryland.
Paul B McCrayDepartment of Pediatrics, Carver College of Medicine, The University of Iowa , Iowa City, Iowa.
Mark ChappellHypertension and Vascular Research Center, Wake Forest School of Medicine , Winston-Salem, North Carolina.
David J HackamDivision of Pediatric Surgery, Department of Surgery, Johns Hopkins University , Baltimore, Maryland.
Hongpeng JiaDivision of Pediatric Surgery, Department of Surgery, Johns Hopkins University , Baltimore, Maryland.
Johns Hopkins University · USUniversity of Iowa · USWake Forest University · US

Funding

Pulmonary Toxicology Facility CoreP30ES005605 · NIEHS · UNIVERSITY OF IOWA · PI Jong Sung Kim · 1990 to 2026
$40.5M
Vector Core-Core 2P30DK054759 · NIDDK · UNIVERSITY OF IOWA · PI Amy Leanne Ryan · 1998 to 2026
$30.5M
SARS-CoV Proteins in Heterologous Viral InfectionP01AI060699 · NIAID · UNIVERSITY OF IOWA · PI PERLMAN, STANLEY · 2004 to 2021
$21.5M
TLR4 Signaling in the Pathogenesis of Surgical Necrotizing EnterocolitisR01GM078238 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI HACKAM, DAVID J · 2006 to 2019
$3.9M
Modulation of TLR4 and TLR9 Signaling in NECR01DK083752 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI HACKAM, DAVID J · 2008 to 2016
$3.4M
NIAID NIH HHS P01 AI060699NIDDK NIH HHS P30 DK054759NIDDK NIH HHS R01 DK083752NIEHS NIH HHS P30 ES005605NIGMS NIH HHS R01 GM078238
6 · The paper itself

Abstract

Angiotensin-converting enzyme 2 (ACE2) is a terminal carboxypeptidase with important functions in the renin-angiotensin system and plays a critical role in inflammatory lung diseases. ACE2 cleaves single-terminal residues from several bioactive peptides such as angiotensin II. However, few of its substrates in the respiratory tract have been identified, and the mechanism underlying the role of ACE2 in inflammatory lung disease has not been fully characterized. In an effort to identify biological targets of ACE2 in the lung, we tested its effects on des-Arg

Indexed as

Angiotensin-Converting Enzyme 2AnimalsAnti-Inflammatory AgentsBradykininCells, CulturedChemokine CXCL5HumansLipopolysaccharidesMiceMice, Inbred C57BLMice, KnockoutNeutrophil InfiltrationPeptidyl-Dipeptidase APneumoniaReceptor, Bradykinin B1TracheaACE2 protein, humanAce2 protein, mouseAngiotensin-Converting Enzyme 2Anti-Inflammatory AgentsBradykininbradykinin, des-Arg(9)-Chemokine CXCL5LipopolysaccharidesPeptidyl-Dipeptidase AReceptor, Bradykinin B1angiotensin-converting enzyme 2bradykinin receptor B1C-X-C motif chemokine 5endotoxinlung inflammation

Identifiers

PMID28935640
PMCPMC5866432
OpenAlexW2756541052

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.