Evidence map›Paper›PMID 30382174›Full record

ArticleScientific reports2018

Pathological cardiac remodeling occurs early in CKD mice from unilateral urinary obstruction, and is attenuated by Enalapril.

Onju Ham, William Jin, Lei Lei, Hui Hui Huang, Kenji Tsuji, Ming Huang, Jason Roh, Anthony Rosenzweig, Hua A Jenny Lu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
2.1field-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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
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  14. Signaling Pathways and Potential Therapeutic Strategies in Cardiac Fibrosis.International journal of molecular sciences · 2023
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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

9 authors at 5 institutions in 2 countries.

Onju HamCenter for Systems Biology, Program in Membrane Biology, Division of Nephrology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, 02114, USA.
William JinCollege of Arts & Sciences, Washington University in St. Louis, St. Louis, MO, 63130, USA.
Lei LeiCenter for Systems Biology, Program in Membrane Biology, Division of Nephrology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, 02114, USA.
Hui Hui HuangCenter for Systems Biology, Program in Membrane Biology, Division of Nephrology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, 02114, USA.
Kenji TsujiCenter for Systems Biology, Program in Membrane Biology, Division of Nephrology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, 02114, USA.
Ming HuangCenter for Systems Biology, Program in Membrane Biology, Division of Nephrology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, 02114, USA.
Jason RohCorrigan Minehan Heart Center, Massachusetts General Hospital and Harvard Medical School, Boston, MA, 02114, USA.
Anthony RosenzweigCorrigan Minehan Heart Center, Massachusetts General Hospital and Harvard Medical School, Boston, MA, 02114, USA.
Hua A Jenny LuCenter for Systems Biology, Program in Membrane Biology, Division of Nephrology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, 02114, USA. halu@partners.org.
Massachusetts General Hospital · USCenter for Systems Biology · USHarvard University · USPeking University · CNWashington University in St. Louis · US

Funding

Pilot & Feasibility ProgramP30DK043351 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI RAYMOND T CHUNG · 1991 to 2026
$35.3M
Transgenic CoreP30DK057521 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI KAHN, BARBARA B. · 2000 to 2019
$31.4M
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
Plasma miRNA predictors of adverse mechanical and electrical remodeling after MIUH3TR000901 · NCATS · MASSACHUSETTS GENERAL HOSPITAL · PI DAS, SAUMYA, KWONG, RAYMOND Y · 2015 to 2017
$3.2M
Does Exercise Induce Cardiomyogenesis?R01HL122987 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI ROSENZWEIG, ANTHONY · 2014 to 2018
$1.7M
Role of miR-222 in pathological hypertrophy and heart failureR01HL135886 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI ROSENZWEIG, ANTHONY · 2017 to 2020
$1.7M
Plasma miRNA predictors of adverse mechanical and electrical remodeling after MIUH2TR000901 · NCATS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI DAS, SAUMYA, KWONG, RAYMOND Y · 2013 to 2014
$1.1M
Role of the novel gene fam4b in phosphatidylserine synthesis in podocytes and maiR21DK092619 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI LU, HUA A · 2012 to 2012
$257k
NCATS NIH HHS UH2 TR000901NCATS NIH HHS UH3 TR000901NHLBI NIH HHS R01 HL122987NHLBI NIH HHS R01 HL135886NIDDK NIH HHS P30 DK043351NIDDK NIH HHS P30 DK057521NIDDK NIH HHS R01 DK096015NIDDK NIH HHS R21 DK092619
6 · The paper itself

Abstract

Cardiovascular disease constitutes the leading cause of mortality in patients with chronic kidney disease (CKD) and end-stage renal disease. Despite increasing recognition of a close interplay between kidney dysfunction and cardiovascular disease, termed cardiorenal syndrome (CRS), the underlying mechanisms of CRS remain poorly understood. Here we report the development of pathological cardiac hypertrophy and fibrosis in early stage non-uremic CKD. Moderate kidney failure was induced three weeks after unilateral urinary obstruction (UUO) in mice. We observed pathological cardiac hypertrophy and increased fibrosis in UUO-induced CKD (UUO/CKD) animals. Further analysis indicated that this cardiac fibrosis was associated with increased expression of transforming growth factor β (TGF-β) along with significant upregulation of Smad 2/3 signaling in the heart. Moreover early treatment of UUO/CKD animals with an angiotensin-converting-enzyme inhibitor (ACE I), Enalapril, significantly attenuated cardiac fibrosis. Enalapril antagonized activation of the TGF-β signaling pathway in the UUO/CKD heart. In summary our study demonstrates the presence of pathological cardiac hypertrophy and fibrosis in mice early in UUO-induced CKD, in association with early activation of the TGF-β/Smad signaling pathway. We also demonstrate the beneficial effect of ACE I in alleviating this early fibrogenic process in the heart in UUO/CKD animals.

Indexed as

Ventricular RemodelingAngiotensin-Converting Enzyme InhibitorsAnimalsBlood PressureCardiomegalyEnalaprilFibrosisHeart VentriclesHypertensionMaleMice, Inbred C57BLOrgan SizeRenal Insufficiency, ChronicSignal TransductionTransforming Growth Factor betaUp-RegulationAngiotensin-Converting Enzyme InhibitorsEnalaprilTransforming Growth Factor beta

Identifiers

PMID30382174
PMCPMC6208335
OpenAlexW2898431436

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LicenceCC BY
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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.