Evidence map›Paper›PMID 29453607›Full record

ArticleClinical and experimental nephrology2018

Semaphorin 7A in circulating regulatory T cells is increased in autosomal-dominant polycystic kidney disease and decreases with tolvaptan treatment.

Yashang Lee, Katrina Lehmann Blount, Feng Dai, Siobhan Thompson, Jonathan Kaufman Scher, Sherrie Bitterman, Madeline Droher, Erica L Herzog, Gilbert Moeckel, Anil Karihaloo and 1 more

Abstract read
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In one paragraph

Article in Clinical and experimental nephrology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 14% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

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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

11 authors at 1 institution in 1 country.

Yashang LeeSection of Nephrology, Yale University School of Medicine, New Haven, CT, 06510, USA.
Katrina Lehmann BlountSection of Nephrology, Yale University School of Medicine, New Haven, CT, 06510, USA.
Feng DaiDepartment of Biostatics, Yale University School of Public Health, 300 George Street, New Haven, CT, 06511, USA.
Siobhan ThompsonSection of Nephrology, Yale University School of Medicine, New Haven, CT, 06510, USA.
Jonathan Kaufman ScherSection of Nephrology, Yale University School of Medicine, New Haven, CT, 06510, USA.
Sherrie BittermanSection of Nephrology, Yale University School of Medicine, New Haven, CT, 06510, USA.
Madeline DroherSection of Nephrology, Yale University School of Medicine, New Haven, CT, 06510, USA.
Erica L HerzogSection of Nephrology, Yale University School of Medicine, New Haven, CT, 06510, USA.
Gilbert MoeckelSection of Nephrology, Yale University School of Medicine, New Haven, CT, 06510, USA.
Anil KarihalooSection of Nephrology, Yale University School of Medicine, New Haven, CT, 06510, USA. Anil.karihaloo@yale.edu.
Neera K DahlSection of Nephrology, Yale University School of Medicine, New Haven, CT, 06510, USA. Neera.dahl@yale.edu.ORCID http://orcid.org/0000-0001-5809-9961
Yale University · US

Funding

Center for Polycystic Kidney Disease Research at YaleP30DK090744 · NIDDK · YALE UNIVERSITY · PI CAPLAN, MICHAEL J. · 2010 to 2014
$5.6M
National Institute of Diabetes and Digestive and Kidney Diseases P30 DK090744
6 · The paper itself

Abstract

backgroundSemaphorin 7A (SEMA7A) is an immunomodulating protein implicated in lung and liver fibrosis. In autosomal-dominant polycystic kidney disease (ADPKD), the progressive expansion of renal cysts, inflammation, and subsequent renal fibrosis leads to end-stage renal disease (ESRD). SEMA7A may play a role in renal fibrosis and in ADPKD.

methodsWe evaluated Sema7a in a mouse model of renal fibrosis and determined the expression of SEMA7A in human ADPKD kidney. We analyzed SEMA7A expression on peripheral blood mononuclear cells (PBMCs), including CD45

resultsSema7a is required for renal fibrosis. SEMA7A shows robust expression in ADPKD kidneys, localizing to cysts derived from distal tubules. SEMA7A is higher in circulating monocytes, but unchanged in CD4

conclusionsSEMA7A shows potential as both a therapeutic target in mammalian kidney fibrosis and as a marker of inflammation in ADPKD patients. SEMA7A expression was lower after tolvaptan treatment, which may reflect drug efficacy.

Indexed as

T-Lymphocytes, RegulatoryAnimalsAntidiuretic Hormone Receptor AntagonistsAntigens, CDFemaleGPI-Linked ProteinsHumansKidneyLeukocytes, MononuclearMaleMiceMiddle AgedPolycystic Kidney, Autosomal DominantSemaphorinsTolvaptanAntidiuretic Hormone Receptor AntagonistsAntigens, CDGPI-Linked ProteinsSEMA7A protein, humanSema7a protein, mouseSemaphorinsTolvaptanADPKDLymphocytesMacrophagesSEMA7A (human)Sema7a (mouse)TolvaptanTregs

Identifiers

PMID29453607
OpenAlexW2790436072

What OpenQuestion holds

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Registered trials

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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.