Evidence map›Paper›PMID 22287584›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2012

Pressure overload-dependent membrane type 1-matrix metalloproteinase induction: relationship to LV remodeling and fibrosis.

Michael R Zile, Catalin F Baicu, Robert E Stroud, An Van Laer, Jazmine Arroyo, Rupak Mukherjee, Jeffrey A Jones, Francis G Spinale

Abstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 4% 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

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

  1. Guidelines for measuring cardiac physiology in mice.American journal of physiology. Heart and circulatory physiology · 2018
    Guideline
  2. Trial
  3. Article
  4. Article
  5. Review
  6. Research Progress of Myocardial Fibrosis and Atrial Fibrillation.Frontiers in cardiovascular medicine · 2022
    Review
  7. Ubiquitin ligaseAmerican journal of physiology. Heart and circulatory physiology · 2021
    Article
  8. Review
  9. miR-133a Replacement Attenuates Thoracic Aortic Aneurysm in Mice.Journal of the American Heart Association · 2021
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

8 authors at 3 institutions in 1 country.

Michael R ZileDivisions of Cardiology, Department of Medicine, Medical University of South Carolina, 29425, USA. zilem@musc.edu
Catalin F Baicu
Robert E Stroud
An Van Laer
Jazmine Arroyo
Rupak Mukherjee
Jeffrey A Jones
Francis G Spinale
Medical University of South Carolina · USRalph H. Johnson VA Medical Center · USWm. Jennings Bryan Dorn VA Medical Center · US

Funding

COLLAGENASE INHIBITION IN HEART FAILURER01HL059165 · NHLBI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI SPINALE, FRANCIS G · 1998 to 2010
$3.2M
Endothelin Receptors and Progression to Heart FailureR01HL057952 · NHLBI · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI SPINALE, FRANCIS G · 1998 to 2011
$3.1M
Myocardial Protection and Matrix ProteasesR01HL095608 · NHLBI · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI SPINALE, FRANCIS G · 2010 to 2013
$1.4M
NHLBI NIH HHS HL-057952NHLBI NIH HHS HL-059165NHLBI NIH HHS HL-095608
6 · The paper itself

Abstract

Increased myocardial extracellular matrix collagen represents an important structural milestone during the development of left ventricular (LV) pressure overload (PO); however, the proteolytic pathways that contribute to this process are not fully understood. This study tested the hypothesis that membrane type 1-matrix metalloproteinase (MT1-MMP) is directly induced at the transcriptional level in vivo during PO and is related to changes in LV collagen content. PO was induced in vivo by transverse aortic constriction in transgenic mice containing the full length human MT1-MMP promoter region ligated to luciferase (MT1-MMP Prom mice). MT1-MMP promoter activation (luciferase expression), expression, and activity; collagen volume fraction (CVF); and left atrial dimension were measured at 1 (n = 8), 2 (n = 12), and 4 (n = 17) wk following PO. Non-PO mice (n = 10) served as controls. Luciferase expression increased by fivefold at 1 wk, fell at 2 wk, and increased again by ninefold at 4 wk of PO (P < 0.05). MT1-MMP expression and activity increased at 1 wk, fell at 2 wk, and increased again at 4 wk after PO. CVF increased at 1 wk, remained unchanged at 2 wk, and increased by threefold at 4 wk of PO (P < 0.05). There was a strong positive correlation between CVF and MT1-MMP activity (r = 0.80, P < 0.05). Left atrial dimension remained unchanged at 1 and 2 wk but increased by 25% at 4 wk of PO. When a mechanical load was applied in vitro to LV papillary muscles isolated from MT1-MMP Prom mice, increased load caused MT1-MMP promoter activation to increase by twofold and MT1-MMP expression to increase by fivefold (P < 0.05). These findings challenge the canonical belief that PO suppresses overall matrix proteolytic activity, but rather supports the concept that certain proteases, such as MT1-MMP, play a pivotal role in PO-induced matrix remodeling and fibrosis.

Indexed as

AnimalsAortic DiseasesBlood PressureBlotting, WesternCollagenEchocardiographyEnzyme InductionExtracellular MatrixFibrosisGene Expression Regulation, EnzymologicHemodynamicsHumansMatrix Metalloproteinase 1MiceMice, TransgenicMyocardiumCollagenMatrix Metalloproteinase 1Neurotransmitter AgentsRNA

Identifiers

PMID22287584
PMCPMC3330784
OpenAlexW2161987480

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.