TY - JOUR
T1 - Myofibroblasts and the extracellular matrix network in post-myocardial infarction cardiac remodeling
AU - Ma, Yonggang
AU - De Castro Brás, Lisandra E.
AU - Toba, Hiroe
AU - Iyer, Rugmani Padmanabhan
AU - Hall, Michael E.
AU - Winniford, Michael D.
AU - Lange, Richard A.
AU - Tyagi, Suresh C.
AU - Lindsey, Merry L.
N1 - Funding Information:
The authors acknowledge support from the American Heart Association 14SDG18860050 to LECB, from the Rapoport Foundation for Cardiovascular Research to RAL, from National Institutes of Health (NIH)/NIH Heart, Lung and Blood Institute HHSN 268201000036C (N01-HV-00244) for the San Antonio Cardiovascular Proteomics Center, R01 HL075360 and HL051971, and from the Biomedical Laboratory Research and Development Service of the Veterans Affairs Office of Research and Development Award 5I01BX000505 to MLL.
PY - 2014/6
Y1 - 2014/6
N2 - The cardiac extracellular matrix (ECM) fills the space between cells, supports tissue organization, and transduces mechanical, chemical, and biological signals to regulate homeostasis of the left ventricle (LV). Following myocardial infarction (MI), a multitude of ECM proteins are synthesized to replace myocyte loss and form a reparative scar. Activated fibroblasts (myofibroblasts) are the primary source of ECM proteins, thus playing a key role in cardiac repair. A balanced turnover of ECM through regulation of synthesis by myofibroblasts and degradation by matrix metalloproteinases (MMPs) is critical for proper scar formation. In this review, we summarize the current literature on the roles of myofibroblasts, MMPs, and ECM proteins in MI-induced LV remodeling. In addition, we discuss future research directions that are needed to further elucidate the molecular mechanisms of ECM actions to optimize cardiac repair.
AB - The cardiac extracellular matrix (ECM) fills the space between cells, supports tissue organization, and transduces mechanical, chemical, and biological signals to regulate homeostasis of the left ventricle (LV). Following myocardial infarction (MI), a multitude of ECM proteins are synthesized to replace myocyte loss and form a reparative scar. Activated fibroblasts (myofibroblasts) are the primary source of ECM proteins, thus playing a key role in cardiac repair. A balanced turnover of ECM through regulation of synthesis by myofibroblasts and degradation by matrix metalloproteinases (MMPs) is critical for proper scar formation. In this review, we summarize the current literature on the roles of myofibroblasts, MMPs, and ECM proteins in MI-induced LV remodeling. In addition, we discuss future research directions that are needed to further elucidate the molecular mechanisms of ECM actions to optimize cardiac repair.
KW - Extracellular matrix
KW - MMP-9
KW - Myocardial infarction
KW - Myofibroblast
KW - Proteomics
KW - Review
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U2 - 10.1007/s00424-014-1463-9
DO - 10.1007/s00424-014-1463-9
M3 - Review article
C2 - 24519465
AN - SCOPUS:84901933884
SN - 0031-6768
VL - 466
SP - 1113
EP - 1127
JO - Pflugers Archiv European Journal of Physiology
JF - Pflugers Archiv European Journal of Physiology
IS - 6
ER -