Evidence map›Paper›PMID 22802913›Full record

ArticleThe open rheumatology journal2012

The Function of SPARC as a Mediator of Fibrosis.

Jessica Trombetta-Esilva, Amy D Bradshaw

Open access · hybridAbstract read
In one paragraph

Article in The open rheumatology journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

49 citing papers in PubMed, 80 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Wound Modulations in Glaucoma Surgery: A Systematic Review.Bioengineering (Basel, Switzerland) · 2024
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Plasma SPARC Elevation in Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Article
  13. Article
  14. Article
  15. Article
  16. Matricellular proteins in cutaneous wound healing.Frontiers in cell and developmental biology · 2022
    Review
  17. Article
  18. Article
  19. Article
  20. 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

2 authors at 2 institutions in 1 country.

Jessica Trombetta-EsilvaDepartment of Craniofacial Biology and Center for Oral Health Research, Medical University of South Carolina, Charleston, SC, USA.
Amy D Bradshaw
Medical University of South Carolina · USRalph H. Johnson VA Medical Center · US

Funding

THE ROLE OF THE RNA BINDING PROTEIN LA IN ORAL TUMOR BIOLOGYP20RR017696 · NCRR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI MITCHELL, HOLLY · 2002 to 2011
$20.7M
T-COHR: Training in Craniofacial and Oral Health ResearchT32DE017551 · NIDCR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI YAO, HAI · 2006 to 2025
$10.3M
Negative Regulation of Innate Immune Responses through MAPK PhosphatasesR01DE018290 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KIRKWOOD, KEITH L · 2007 to 2011
$1.8M
MUSC Short-Term Research Education Program to Increase DiversityR25HL092611 · NHLBI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI WRIGHT, CYNTHIA F. · 2008 to 2022
$1.5M
Post-Synthetic Procollagen Processing in Load-Induced Left Ventricular RemodelingR01HL094517 · NHLBI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BRADSHAW, AMY D · 2009 to 2010
$738k
The Role of SPARC in Procollagen Processing in the Periodontal LigamentF30DE023009 · NIDCR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI TROMBETTA-ESILVA, JESSICA MARIE · 2012 to 2015
$183k
NCRR NIH HHS P20 RR017696NHLBI NIH HHS R01 HL094517NHLBI NIH HHS R25 HL092611NIDCR NIH HHS F30 DE023009NIDCR NIH HHS R01 DE018290NIDCR NIH HHS T32 DE017551
6 · The paper itself

Abstract

Fibrosis is a common end-point of a number of different diseases such as hypertension, diabetes, liver cirrhosis, and those associated with chronic inflammation. Fibrosis is characterized by excessive deposition of extracellular matrix that interferes with normal tissue architecture and function. Increased expression of secreted protein acidic and rich in cysteine (SPARC) in fibrotic tissues has been reported in numerous studies. SPARC is a 43 kDa collagen-binding protein secreted from several different cell types into the extracellular matrix and has been shown to be anti-proliferative and counter-adhesive in vitro. SPARC is a matricellular protein; meaning SPARC is secreted into the extracellular space but does not serve a structural function. Instead, SPARC modulates interactions between cells and the surrounding extracellular matrix. In animal models of fibrotic disease and in human fibrotic tissues, elevated expression of SPARC has been reported in many tissues including heart, lungs, kidneys, liver, dermis, intestine, and eyes. In this review, we will summarize current studies that have examined the expression and functional importance of SPARC in various animal models of fibrosis and in human tissues. Although cellular mechanisms of SPARC in fibrosis remain to be fully elucidated, the studies summarized here provide impetus to further explore the efficacy of SPARC as a potential target for reducing fibrosis.

Indexed as

Collagendisease.extracellular matrixmatricellular protein

Identifiers

PMID22802913
PMCPMC3395844
OpenAlexW2140698023

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.