Evidence map›Paper›PMID 36149056›Full record

ArticleeLife2022

Consequences of PDGFRα

Jill T Kuwabara, Akitoshi Hara, Sumit Bhutada, Greg S Gojanovich, Jasmine Chen, Kanani Hokutan, Vikram Shettigar, Anson Y Lee, Lydia P DeAngelo, Jack R Heckl and 5 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

29 citing papers in PubMed, 41 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

15 authors at 3 institutions in 1 country.

Jill T Kuwabara *Center for Cardiovascular Research, John A. Burns School of Medicine, University of Hawaii at Manoa, Honolulu, United States.
Akitoshi Hara *Center for Cardiovascular Research, John A. Burns School of Medicine, University of Hawaii at Manoa, Honolulu, United States.
Sumit BhutadaDepartment of Biomedical Engineering, Cleveland Clinic Lerner Research Institute, Cleveland, United States.ORCID 0000-0002-5274-5122
Greg S GojanovichCenter for Cardiovascular Research, John A. Burns School of Medicine, University of Hawaii at Manoa, Honolulu, United States.
Jasmine ChenCenter for Cardiovascular Research, John A. Burns School of Medicine, University of Hawaii at Manoa, Honolulu, United States.
Kanani HokutanCenter for Cardiovascular Research, John A. Burns School of Medicine, University of Hawaii at Manoa, Honolulu, United States.
Vikram ShettigarDorothy M. Davis Heart and Lung Research Institute, Department of Physiology and Cell Biology, The Ohio State University Wexner Medical Center, Columbus, United States.
Anson Y LeeCenter for Cardiovascular Research, John A. Burns School of Medicine, University of Hawaii at Manoa, Honolulu, United States.
Lydia P DeAngeloCenter for Cardiovascular Research, John A. Burns School of Medicine, University of Hawaii at Manoa, Honolulu, United States.ORCID 0000-0002-0549-325X
Jack R HecklCenter for Cardiovascular Research, John A. Burns School of Medicine, University of Hawaii at Manoa, Honolulu, United States.
Julia R JahansoozCenter for Cardiovascular Research, John A. Burns School of Medicine, University of Hawaii at Manoa, Honolulu, United States.
Dillon K TacdolCenter for Cardiovascular Research, John A. Burns School of Medicine, University of Hawaii at Manoa, Honolulu, United States.
Mark T ZioloDorothy M. Davis Heart and Lung Research Institute, Department of Physiology and Cell Biology, The Ohio State University Wexner Medical Center, Columbus, United States.
Suneel S ApteDepartment of Biomedical Engineering, Cleveland Clinic Lerner Research Institute, Cleveland, United States.ORCID 0000-0001-8441-1226
Michelle D TallquistCenter for Cardiovascular Research, John A. Burns School of Medicine, University of Hawaii at Manoa, Honolulu, United States.ORCID 0000-0002-1383-144X
University of Hawaiʻi at Mānoa · USCleveland Clinic Lerner College of Medicine · USThe Ohio State University Wexner Medical Center · US

Funding

University of Hawaii Cancer Center CCSGP30CA071789 · NCI · UNIVERSITY OF HAWAII AT MANOA · PI GERTRAUD MASKARINEC · 1996 to 2026
$56.2M
RESEARCH DESIGN, BIOSTATISTICS AND RESEARCH ETHICS COREG12MD007601 · NIMHD · UNIVERSITY OF HAWAII AT MANOA · PI BERRY, MARLA J · 2012 to 2016
$13.0M
Pilot Project ProgramP30GM103341 · NIGMS · UNIVERSITY OF HAWAII AT MANOA · PI SHOHET, RALPH V. · 2012 to 2016
$5.5M
Training in Cardiovascular Research at the University of HawaiiT32HL115505 · NHLBI · UNIVERSITY OF HAWAII AT MANOA · PI Michelle D Tallquist · 2012 to 2026
$3.8M
PDGF Receptor Signaling in Mammalian DevelopmentR01HL074257 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI TALLQUIST, MICHELLE D · 2003 to 2014
$3.7M
Regulation of cardiac inflammation by fibroblastsR01HL144067 · NHLBI · UNIVERSITY OF HAWAII AT MANOA · PI TALLQUIST, MICHELLE D · 2018 to 2021
$2.3M
High-End Instrumentation (HEI) Grant Program (S10)S10OD023436 · OD · CLEVELAND CLINIC LERNER COM-CWRU · PI WILLARD, BELINDA BELLE · 2017 to 2017
$873k
Live-Cell Imaging System with TIRF and PhotomanipulationS10OD028515 · OD · UNIVERSITY OF HAWAII AT MANOA · PI FARRAR, CHRISTINE · 2020 to 2020
$382k
NCI NIH HHS P30 CA071789NHLBI NIH HHS R01 HL074257NHLBI NIH HHS R01 HL144067NHLBI NIH HHS T32 HL115505NIGMS NIH HHS P30 GM103341NIH HHS S10 OD023436NIH HHS S10 OD028515NIMHD NIH HHS G12 MD007601
6 · The paper itself

Abstract

Fibroblasts produce the majority of collagen in the heart and are thought to regulate extracellular matrix (ECM) turnover. Although fibrosis accompanies many cardiac pathologies and is generally deleterious, the role of fibroblasts in maintaining the basal ECM network and in fibrosis in vivo is poorly understood. We genetically ablated fibroblasts in mice to evaluate the impact on homeostasis of adult ECM and cardiac function after injury. Fibroblast-ablated mice demonstrated a substantive reduction in cardiac fibroblasts, but fibrillar collagen and the ECM proteome were not overtly altered when evaluated by quantitative mass spectrometry and N-terminomics. However, the distribution and quantity of collagen VI, microfibrillar collagen that forms an open network with the basement membrane, was reduced. In fibroblast-ablated mice, cardiac function was better preserved following angiotensin II/phenylephrine (AngII/PE)-induced fibrosis and myocardial infarction (MI). Analysis of cardiomyocyte function demonstrated altered sarcomere shortening and slowed calcium decline in both uninjured and AngII/PE-infused fibroblast-ablated mice. After MI, the residual resident fibroblasts responded to injury, albeit with reduced proliferation and numbers immediately after injury. These results indicate that the adult mouse heart tolerates a significant degree of fibroblast loss with a potentially beneficial impact on cardiac function after injury. The cardioprotective effect of controlled fibroblast reduction may have therapeutic value in heart disease.

Indexed as

Myocardial InfarctionReceptor, Platelet-Derived Growth Factor alphaAngiotensin IIAnimalsCalciumCollagenFibroblastsFibrosisMiceMyocardiumPhenylephrineProteomeAngiotensin IICalciumCollagenPhenylephrineProteomeReceptor, Platelet-Derived Growth Factor alphacell biologyextracellular matrixfibroblasthomeostasismouse

Identifiers

PMID36149056
PMCPMC9576271
OpenAlexW4296805857

What OpenQuestion holds

Textmetadata
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.