Cited by 113Cardiac Fibrosis and RemodelingProtease and Inhibitor MechanismsSignaling Pathways in Disease

Matrix metalloproteinases as input and output signals for post-myocardial infarction remodeling

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Lindsey, Merry L., Iyer, Rugmani Padmanabhan, Jung, Mira, DeLeon-Pennell, Kristine Y., Ma, Yonggang·2016·Journal of Molecular and Cellular Cardiology

Abstract

Despite current optimal therapeutic regimens, approximately one in four patients diagnosed with myocardial infarction (MI) will go on to develop congestive heart failure, and heart failure has a high five-year mortality rate of 50%. Elucidating mechanisms whereby heart failure develops post-MI, therefore, is highly needed. Matrix metalloproteinases (MMPs) are key enzymes involved in post-MI remodeling of the left ventricle (LV). While MMPs process cytokine and extracellular matrix (ECM) substrates to regulate the inflammatory and fibrotic components of the wound healing response to MI, MMPs also serve as upstream signaling initiators with direct actions on cell signaling cascades. In this review, we summarize the current literature regarding MMP roles in post-MI LV remodeling. We also identify the current knowledge gaps and provide templates for experiments to fill these gaps. A more complete understanding of MMP roles, particularly with regards to upstream signaling roles, may provide new strategies to limit adverse LV remodeling.

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Crossref · 10.1016/j.yjmcc.2015.12.018

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  • Myofibroblasts continuously regulate matrix deposition and turnover through the actions of MMPs and TIMPs.

    “Myofibroblasts continuously regulate matrix deposition and turnover through the actions of MMPs and tissue inhibitors of metalloproteinases (TIMPs).117”
  • Inflammatory monocytes and tissue-resident macrophages are key regulators of tissue fibrosis, playing major roles in the initiation, maintenance, and resolution of tissue injury.

    “Inflammatory monocytes and tissue-resident macrophages are key regulators of tissue fibrosis, playing major roles in the initiation, maintenance and resolution of tissue injury58–60.”

    From Fibrosis: from mechanisms to medicines (2020) · cites this paper as [58]

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Research works printed but not linked: 7

  1. [34]Lindsey ML Escobar GP Dobrucki LW Goshorn DK Bouges S Mingoia JT Matrix metalloproteinase-9 gene deletion facilitates angiogenesis after myocardial infarction American journal of physiology: Heart and circulatory physiology 2006 290 H232 9 16126817
  2. [37]Ma Y Halade GV Zhang J Ramirez TA Levin D Voorhees A Matrix metalloproteinase-28 deletion exacerbates cardiac dysfunction and rupture after myocardial infarction in mice by inhibiting M2 macrophage activation Circulation research 2013 112 675 88 23261783 PMC3597388
  3. [38]Lindsey ML Zamilpa R Temporal and spatial expression of matrix metalloproteinases and tissue inhibitors of metalloproteinases following myocardial infarction Cardiovascular therapeutics 2012 30 31 41 20645986 PMC2972388
  4. [53]Zamilpa R Ibarra J de Castro Bras LE Ramirez TA Nguyen N Halade GV Transgenic overexpression of matrix metalloproteinase-9 in macrophages attenuates the inflammatory response and improves left ventricular function post-myocardial infarction Journal of molecular and cellular cardiology 2012 53 599 608 22884843 PMC3472138
  5. [63]Zamilpa R Lopez EF Chiao YA Dai Q Escobar GP Hakala K Proteomic analysis identifies in vivo candidate matrix metalloproteinase-9 substrates in the left ventricle post-myocardial infarction Proteomics 2010 10 2214 23 20354994 PMC3017347
  6. [65]Chiao YA Zamilpa R Lopez EF Dai Q Escobar GP Hakala KW In vivo Matrix Metalloproteinase-7 Substrates Identified in the Left Ventricle Post-Myocardial Infarction Using Proteomics Journal of proteome research 2010 9 2649 57 20232908 PMC2866015
  7. [92]Lindsey ML Iyer RP Zamilpa R Yabluchanskiy A DeLeon-Pennell KY Hall ME A Novel Collagen Matricryptin Reduces Left Ventricular Dilation Post-Myocardial Infarction by Promoting Scar Formation and Angiogenesis J Am Coll Cardiol 2015 in press PMC4575409 26383724

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Authors
Lindsey, M. L., Iyer, R. P., Jung, M., DeLeon-Pennell, K. Y., & Ma, Y.
Affiliations
University of Mississippi Medical Center (US)
Corresponding author
  • Lindsey, Merry L.
  • Ma, Yonggang
Venue
Journal of Molecular and Cellular Cardiology
Publisher
Elsevier BV
Published
2016-02
Volume
91
Pages
134-140
ISSN
0022-2828 (ISSN-L)
OpenAlex
W2212574418
Cited by
113
References
92
Citations by year
2026: 8 · 2025: 6 · 2024: 4 · 2023: 9 · 2022: 10 · 2021: 9 · 2020: 13 · 2019: 8 · 2018: 16 · 2017: 13 · 2016: 10 · 2015: 7
FWCI
2.64
Type
journal article
Language
en
Open access
Locations
  • Journal of Molecular and Cellular Cardiology (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • U.S. Department of Veterans Affairs (I01BX000505)
  • American Heart Association
  • Office of Research and Development
  • National Institutes of Health
  • U.S. Public Health Service (HHSN-268201000036C)
  • National Heart, Lung, and Blood Institute (N01-HV-00244, HL075360, R01HL075360, HHSN268201000036C, P01HL051971)
  • National Institute of General Medical Sciences (U54GM114833, GM114833, P20GM104357)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Protease and Inhibitor Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
Keywords
matrix metalloproteinases, myocardial infarction, left ventricular remodeling, heart failure, extracellular matrix, cytokine processing, fibrosis, inflammation, signal transduction, wound healing
MeSH terms
Animals, Extracellular Matrix, Gene Expression Regulation, Heart Failure, Humans, Isoenzymes, Myocardial Infarction, Myocardium, Wound Healing, Signal Transduction, Cytokines, Extracellular Matrix Proteins, Ventricular Remodeling, Matrix Metalloproteinases, Proteomics

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