TY - JOUR
T1 - Matrix metalloproteinases as input and output signals for post-myocardial infarction remodeling
AU - Lindsey, Merry L.
AU - Iyer, Rugmani Padmanabhan
AU - Jung, Mira
AU - DeLeon-Pennell, Kristine Y.
AU - Ma, Yonggang
N1 - Funding Information:
This work was supported by the National Institutes of Health HHSN 268201000036C (N01-HV-00244), HL075360, and GM114833, and the Biomedical Laboratory Research and Development Service of the Veterans Affairs Office of Research and Development Award 5I01BX000505 to MLL; American Heart Association Postdoctoral Grant 14POST18770012 to RPI and Scientist Development Grant 15SDG22930009 to YM; and P01HL051971 and P20GM104357.
Publisher Copyright:
© 2015 Elsevier Ltd.
PY - 2016/2/1
Y1 - 2016/2/1
N2 - 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.
AB - 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.
KW - Extracellular matridomics
KW - Extracellular matrix
KW - MMP
KW - Proteomics
KW - Signaling
KW - Systems biology
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U2 - 10.1016/j.yjmcc.2015.12.018
DO - 10.1016/j.yjmcc.2015.12.018
M3 - Review article
C2 - 26721597
AN - SCOPUS:84953433030
VL - 91
SP - 134
EP - 140
JO - Journal of Molecular and Cellular Cardiology
JF - Journal of Molecular and Cellular Cardiology
SN - 0022-2828
ER -