Evidence map›Paper›PMID 22464947›Full record

ArticleThe American journal of pathology2012

MT1-MMP-dependent remodeling of cardiac extracellular matrix structure and function following myocardial infarction.

Gerald C Koenig, R Grant Rowe, Sharlene M Day, Farideh Sabeh, Jeffrey J Atkinson, Kenneth R Cooke, Stephen J Weiss

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. The regenerative response of cardiac interstitial cells.Journal of molecular cell biology · 2023
    Article
  6. Article
  7. Review
  8. Article
  9. Crosstalk between Calcium and ROS in Pathophysiological Conditions.Oxidative medicine and cellular longevity · 2019
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Matrix metalloproteinase collagenolysis in health and disease.Biochimica et biophysica acta. Molecular cell research · 2017
    Review
  15. Review
  16. Article
  17. MMP-9 signaling in the left ventricle following myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2016
    Review
  18. Modifying the mechanics of healing infarcts: Is better the enemy of good?Journal of molecular and cellular cardiology · 2016
    Review
  19. Article
  20. Matrix metalloproteinases as therapeutic targets for idiopathic pulmonary fibrosis.American journal of respiratory cell and molecular biology · 2015
    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

7 authors at 2 institutions in 3 countries.

Gerald C KoenigDivision of Cardiovascular Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan 48109-2216, USA.
R Grant Rowe
Sharlene M Day
Farideh Sabeh
Jeffrey J Atkinson
Kenneth R Cooke
Stephen J Weiss
University of Michigan–Ann Arbor · USPulmonary Associates · US

Funding

FUNCTION OF THE MEMBRANE TYPE MATRIX METALLOPROTEINASER01CA071699 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WEISS, STEPHEN J · 1997 to 2024
$7.3M
METALLOPROTEASE DEPENDENT FIBRINOLYSIS AND ANGIOGENESISR01CA088308 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WEISS, STEPHEN J · 2000 to 2015
$4.6M
NCI NIH HHS 5R01CA71699NCI NIH HHS 5R01CA88308NCI NIH HHS R01 CA071699NCI NIH HHS R01 CA088308NHLBI NIH HHS R01HL09338
6 · The paper itself

Abstract

The myocardial extracellular matrix (ECM), an interwoven meshwork of proteins, glycoproteins, proteoglycans, and glycosaminoglycans that is dominated by polymeric fibrils of type I collagen, serves as the mechanical scaffold on which myocytes are arrayed for coordinated and synergistic force transduction. Following ischemic injury, cardiac ECM remodeling is initiated via localized proteolysis, the bulk of which has been assigned to matrix metalloproteinase (MMP) family members. Nevertheless, the key effector(s) of myocardial type I collagenolysis both in vitro and in vivo have remained unidentified. In this study, using cardiac explants from mice deficient in each of the major type I collagenolytic MMPs, including MMP-13, MMP-8, MMP-2, MMP-9, or MT1-MMP, we identify the membrane-anchored MMP, MT1-MMP, as the dominant collagenase that is operative within myocardial tissues in vitro. Extending these observations to an in vivo setting, mice heterozygous for an MT1-MMP-null allele display a distinct survival advantage and retain myocardial function relative to wild-type littermates in an experimental model of myocardial infarction, effects associated with preservation of the myocardial type I collagen network as a consequence of the decreased collagenolytic potential of cardiac fibroblasts. This study identifies MT1-MMP as a key MMP responsible for effecting postinfarction cardiac ECM remodeling and cardiac dysfunction.

Indexed as

AnimalsCollagen Type IExtracellular MatrixFemaleFibroblastsIn Situ HybridizationMatrix Metalloproteinase 14MiceMice, Inbred C57BLMice, KnockoutMyocardial InfarctionMyocardial IschemiaOrgan Culture TechniquesUltrasonographyVentricular RemodelingCollagen Type IMatrix Metalloproteinase 14

Identifiers

PMID22464947
PMCPMC3349831
OpenAlexW2059039052

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.