Evidence map›Paper›PMID 26080361›Full record

ArticleJournal of molecular and cellular cardiology2015

Building a better infarct: Modulation of collagen cross-linking to increase infarct stiffness and reduce left ventricular dilation post-myocardial infarction.

Andrew P Voorhees, Kristine Y DeLeon-Pennell, Yonggang Ma, Ganesh V Halade, Andriy Yabluchanskiy, Rugmani Padmanabhan Iyer, Elizabeth Flynn, Courtney A Cates, Merry L Lindsey, Hai-Chao Han

Abstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 2 pooled it
7.0field-weighted citation impact, top 2% 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

46 citing papers in PubMed, 2 syntheses or guidelines pooled it, 66 citations in OpenAlex.

  1. Guidelines for measuring cardiac physiology in mice.American journal of physiology. Heart and circulatory physiology · 2018
    Guideline
  2. Guidelines for experimental models of myocardial ischemia and infarction.American journal of physiology. Heart and circulatory physiology · 2018
    Guideline
  3. Cardio-Vascular Extracellular Matrix: The Unmet Enigma.International journal of molecular sciences · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Dynamic and static biomechanical traits of cardiac fibrosis.Frontiers in bioengineering and biotechnology · 2022
    Review
  9. Article
  10. ChronicAmerican journal of physiology. Heart and circulatory physiology · 2021
    Article
  11. Review
  12. Find the stimulus, save the heart: a heroes' story.American journal of physiology. Heart and circulatory physiology · 2021
    Article
  13. Review
  14. Review
  15. Article
  16. Cardiac Fibroblasts and Myocardial Regeneration.Frontiers in bioengineering and biotechnology · 2021
    Review
  17. Review
  18. Cardiac fibroblast activation during myocardial infarction wound healing: Fibroblast polarization after MI.Matrix biology : journal of the International Society for Matrix Biology · 2020
    Review
  19. Article
  20. CD8American journal of physiology. Heart and circulatory physiology · 2019
    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

10 authors at 1 institution in 1 country.

Andrew P VoorheesDepartment of Mechanical Engineering, The University of Texas at San Antonio, USA; Joint Biomedical Engineering Program, UTSA-UTHSCSA, USA; San Antonio Cardiovascular Proteomics Center, USA.
Kristine Y DeLeon-PennellSan Antonio Cardiovascular Proteomics Center, USA; Mississippi Center for Heart Research, Department of Physiology and Biophysics, University of Mississippi Medical Center, USA.
Yonggang MaSan Antonio Cardiovascular Proteomics Center, USA; Mississippi Center for Heart Research, Department of Physiology and Biophysics, University of Mississippi Medical Center, USA.
Ganesh V HaladeSan Antonio Cardiovascular Proteomics Center, USA; Division of Cardiovascular Disease, Department of Medicine, The University of Alabama at Birmingham, USA.
Andriy YabluchanskiySan Antonio Cardiovascular Proteomics Center, USA; Mississippi Center for Heart Research, Department of Physiology and Biophysics, University of Mississippi Medical Center, USA; Research Service, G.V. (Sonny) Montgomery Veterans Affairs Medical Center, USA.
Rugmani Padmanabhan IyerSan Antonio Cardiovascular Proteomics Center, USA; Mississippi Center for Heart Research, Department of Physiology and Biophysics, University of Mississippi Medical Center, USA.
Elizabeth FlynnMississippi Center for Heart Research, Department of Physiology and Biophysics, University of Mississippi Medical Center, USA.
Courtney A CatesMississippi Center for Heart Research, Department of Physiology and Biophysics, University of Mississippi Medical Center, USA.
Merry L LindseyJoint Biomedical Engineering Program, UTSA-UTHSCSA, USA; San Antonio Cardiovascular Proteomics Center, USA; Mississippi Center for Heart Research, Department of Physiology and Biophysics, University of Mississippi Medical Center, USA; Research Service, G.V. (Sonny) Montgomery Veterans Affairs Medical Center, USA.
Hai-Chao HanDepartment of Mechanical Engineering, The University of Texas at San Antonio, USA; Joint Biomedical Engineering Program, UTSA-UTHSCSA, USA; San Antonio Cardiovascular Proteomics Center, USA. Electronic address: hchan@utsa.edu.
University of Mississippi Medical Center · US

Funding

STRUCTURAL VASCULAR ADAPTATION OF THE MICROCIRCULATIONP01HL051971 · NHLBI · UNIVERSITY OF MISSISSIPPI MEDICAL CENTER · PI HALL, JOHN E · 1993 to 2018
$39.4M
The role of leptin in autoimmune-associated hypertensionP20GM104357 · NIGMS · UNIVERSITY OF MISSISSIPPI MED CTR · PI TAYLOR, ERIN BASSFORD · 2013 to 2022
$23.4M
PATHOBIOLOGY OF OCCLUSIVE VASCULAR DISEASET32HL007446 · NHLBI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Jean Chrisostome Bopassa · 1985 to 2026
$8.9M
The Role of Macrophage-derived MMPs in LV RemodelingR01HL075360 · NHLBI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI LINDSEY, MERRY L. · 2004 to 2018
$5.4M
Biomechanical Mechanisms of Artery TortuosityR01HL095852 · NHLBI · UNIVERSITY OF TEXAS SAN ANTONIO · PI HAN, HAI-CHAO · 2010 to 2014
$1.8M
DHA Mechanisms in Obesity-mediated Cardiac Remodeling Post-Myocardial InfarctionK99AT006704 · NCCIH · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI HALADE, GANESH V · 2011 to 2012
$194k
Neutrophil Polarization Following Myocardial InfarctionI01BX000505 · VA · VETERANS HEALTH ADMINISTRATION · PI LINDSEY, MERRY L. · 2009 to 2024
–
BLRD VA I01 BX000505NCCIH NIH HHS K99 AT006704NCCIH NIH HHS K99-AT006704NHLBI NIH HHS HHSN268201000036CNHLBI NIH HHS HL051971NHLBI NIH HHS N01-HV-00244NHLBI NIH HHS P01 HL051971NHLBI NIH HHS R01 HL075360NHLBI NIH HHS R01HL075360NHLBI NIH HHS R01 HL095852NHLBI NIH HHS R01HL095852NHLBI NIH HHS T32 HL007446NIGMS NIH HHS GM104357NIGMS NIH HHS P20 GM104357PHS HHS HHSN 268201000036C
6 · The paper itself

Abstract

Matrix metalloproteinase-9 (MMP-9) deletion attenuates collagen accumulation and dilation of the left ventricle (LV) post-myocardial infarction (MI); however the biomechanical mechanisms underlying the improved outcome are poorly understood. The aim of this study was to determine the mechanisms whereby MMP-9 deletion alters collagen network composition and assembly in the LV post-MI to modulate the mechanical properties of myocardial scar tissue. Adult C57BL/6J wild-type (WT; n=88) and MMP-9 null (MMP-9(-/-); n=92) mice of both sexes underwent permanent coronary artery ligation and were compared to day 0 controls (n=42). At day 7 post-MI, WT LVs displayed a 3-fold increase in end-diastolic volume, while MMP-9(-/-) showed only a 2-fold increase (p<0.05). Biaxial mechanical testing revealed that MMP-9(-/-) infarcts were stiffer than WT infarcts, as indicated by a 1.3-fold reduction in predicted in vivo circumferential stretch (p<0.05). Paradoxically, MMP-9(-/-) infarcts had a 1.8-fold reduction in collagen deposition (p<0.05). This apparent contradiction was explained by a 3.1-fold increase in lysyl oxidase (p<0.05) in MMP-9(-/-) infarcts, indicating that MMP-9 deletion increased collagen cross-linking activity. Furthermore, MMP-9 deletion led to a 3.0-fold increase in bone morphogenetic protein-1, the metalloproteinase that cleaves pro-collagen and pro-lysyl oxidase (p<0.05) and reduced fibronectin fragmentation by 49% (p<0.05) to enhance lysyl oxidase activity. We conclude that MMP-9 deletion increases infarct stiffness and prevents LV dilation by reducing collagen degradation and facilitating collagen assembly and cross-linking through preservation of the fibronectin network and activation of lysyl oxidase.

Indexed as

Ventricular RemodelingAnimalsCardiac VolumeCollagenFemaleHeart VentriclesMaleMatrix Metalloproteinase 9Mice, Inbred C57BLMice, KnockoutMyocardial InfarctionMyocardiumVentricular Function, LeftCollagenMatrix Metalloproteinase 9Mmp9 protein, mouseCardiac mechanicsCollagen crosslinkingInfarct stiffnessLysyl oxidaseMatrix metalloproteinase-9Proteomics

Identifiers

PMID26080361
PMCPMC4530076
OpenAlexW1915631039

What OpenQuestion holds

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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.