Evidence map›Paper›PMID 26582465›Full record

ReviewJournal of molecular and cellular cardiology2016

The role of secreted protein acidic and rich in cysteine (SPARC) in cardiac repair and fibrosis: Does expression of SPARC by macrophages influence outcomes?

Amy D Bradshaw

Open access · greenAbstract readReview
In one paragraph

Review in Journal of molecular and cellular cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

35 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Review
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  14. Article
  15. Diabetic fibrosis.Biochimica et biophysica acta. Molecular basis of disease · 2021
    Review
  16. Article
  17. SPARC production by bone marrow-derived cells contributes to myocardial fibrosis in pressure overload.American journal of physiology. Heart and circulatory physiology · 2021
    Article
  18. Article
  19. Article
  20. Critical roles of macrophages in pressure overload-induced cardiac remodeling.Journal of molecular medicine (Berlin, Germany) · 2021
    Review
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

1 author at 1 institution in 1 country.

Amy D BradshawGazes Cardiac Research Institute, Division of Cardiology, Department of Medicine, Medical University of South Carolina, MSC 773, Charleston, SC 29425, United States; Ralph H. Johnson Department of Veterans Affairs Medical Center, Charleston, SC, United States. Electronic address: bradshad@musc.edu.
Medical University of South Carolina · US

Funding

Procollagen Binding Proteins in Age-Dependent LV RemodelingI01BX001385 · VA · RALPH H JOHNSON VA MEDICAL CENTER · PI BRADSHAW, AMY D · 2012 to 2015
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BLRD VA I01 BX001385
6 · The paper itself

Abstract

Secreted protein acidic and rich in cysteine (SPARC) is a matricellular, collagen-binding protein. Matricellular proteins are described as extracellular matrix-associated proteins that do not serve classical structural roles in the matrix such as those ascribed to laminins and collagens. The family of matricellular proteins modulates cell:extracellular matrix interactions and is actively expressed during tissue remodeling. Functional activities attributed to SPARC in cultured cells include regulation of cell adhesion, cytoskeletal rearrangement, proliferation, and matrix assembly. The primary phenotype characteristic of SPARC-null mice is a deficit in amounts of fibrillar collagen and fibril morphology. Strikingly, SPARC-null mice demonstrate a blunted fibrotic response in a number of different tissue settings. The role of monocyte/macrophages as an important component of tissue fibrosis is becoming increasingly appreciated. Expression of SPARC by bone marrow derived inflammatory cells raises the interesting proposition that SPARC produced by infiltrating leukocytes might contribute to the course of inflammation and tissue fibrosis in the heart. This review will summarize results from studies defining the function of SPARC in myocardial repair and fibrosis and results from other non-cardiac tissues that shed light onto possible consequences of SPARC expression by monocyte/macrophages in the setting of heart disease.

Indexed as

Gene ExpressionWound HealingAge FactorsAnimalsBlood PressureChemotaxis, LeukocyteFibrosisHumansMacrophage ActivationMacrophagesMechanical PhenomenaMechanotransduction, CellularMyocardial InfarctionMyocarditisMyocardiumOsteonectinOsteonectinSPARC protein, humanBM40CollagenExtracellular matrixInflammationMatricellularOsteonectin

Identifiers

PMID26582465
PMCPMC12997076
OpenAlexW2175224364

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.