Evidence map›Paper›PMID 28701310›Full record

ArticleAmerican journal of physiology. Renal physiology2017

Deletion of β1-integrin in collecting duct principal cells leads to tubular injury and renal medullary fibrosis.

Fahmy A Mamuya, Dongping Xie, Lei Lei, Ming Huang, Kenji Tsuji, Diane E Capen, BaoXue Yang, Ralph Weissleder, Teodor G Păunescu, Hua A Jenny Lu

Open access · greenAbstract read
In one paragraph

Article 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 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 20% 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, 26 citations in OpenAlex.

  1. Article
  2. Novel Drug Targets in Diastolic Heart Disease.International journal of molecular sciences · 2025
    Review
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  10. Loss of ELK1 has differential effects on age-dependent organ fibrosis.The international journal of biochemistry & cell biology · 2020
    Article
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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

10 authors at 4 institutions in 2 countries.

Fahmy A MamuyaProgram in Membrane Biology and Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts.
Dongping XieProgram in Membrane Biology and Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts.
Lei LeiProgram in Membrane Biology and Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts.
Ming HuangProgram in Membrane Biology and Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts.
Kenji TsujiProgram in Membrane Biology and Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts.
Diane E CapenProgram in Membrane Biology and Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts.
BaoXue YangDepartment of Pharmacology, School of Basic Medical Sciences, Peking University, Beijing, China.
Ralph WeisslederCenter for Systems Biology, Massachusetts General Hospital, Boston, Massachusetts.
Teodor G PăunescuProgram in Membrane Biology and Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts.
Hua A Jenny LuProgram in Membrane Biology and Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts; Lu.Hua@mgh.harvard.edu.
Center for Systems Biology · USMassachusetts General Hospital · USHarvard University · USPeking University · CN

Funding

Transgenic CoreP30DK057521 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI KAHN, BARBARA B. · 2000 to 2019
$31.4M
SIGNALLING IN MESANGIAL CELLS--CALCIUM AND PHOPHOLIPASESP01DK038452 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI BROWN, DENNIS · 1987 to 2012
$20.1M
Training Grant in Molecular Imaging Research (MGH/HMS)T32CA079443 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI WEISSLEDER, MD, PHD, RALPH · 2000 to 2025
$10.1M
Novel roles of integrin b1 signaling in regulating principal cell function andmaintaining collecting duct integrityR01DK096015 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI LU, HUA A · 2013 to 2022
$3.7M
NCI NIH HHS T32 CA079443NIDDK NIH HHS P01 DK038452NIDDK NIH HHS P30 DK057521NIDDK NIH HHS R01 DK096015
6 · The paper itself

Abstract

The renal collecting duct (CD) contains two major cell types, intercalated (ICs) and principal cells (PCs). A previous report showed that deletion of β1-integrin in the entire renal CD causes defective CD morphogenesis resulting in kidney dysfunction. However, subsequent deletion of β1-integrin specifically in ICs and PCs, respectively, did not cause any morphological defects in the CDs. The discrepancy between these studies prompts us to reinvestigate the role of β1-integrin in CD cells, specifically in the PCs. We conditionally deleted β1-integrin in mouse CD PCs using a specific aquaporin-2 (AQP2) promoter Cre-LoxP system. The resulting mutant mice, β-1

Indexed as

Gene DeletionAge FactorsAnimalsApoptosisAquaporin 2Cell ProliferationExtracellular MatrixFailure to ThriveFibrosisGenetic Predisposition to DiseaseIntegrasesIntegrin beta1Kidney MedullaKidney Tubules, CollectingMice, KnockoutPhenotypeAqp2 protein, mouseAquaporin 2Cre recombinaseIntegrasesIntegrin beta1Protein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type ISmad2 ProteinSmad2 protein, mouseTransforming Growth Factor betaaquaporin-2collecting ductsrenal fibrosisTGF-ββ1-integrins

Identifiers

PMID28701310
PMCPMC5668581
OpenAlexW2734878221

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.