Extracellular Matrix and Fibroblast Communication Following Myocardial Infarction

Yonggang Ma; Ganesh V. Halade; Merry L. Lindsey

doi:10.1007/s12265-012-9398-z

Extracellular Matrix and Fibroblast Communication Following Myocardial Infarction

Yonggang Ma, Ganesh V. Halade, Merry L. Lindsey

Research output: Contribution to journal › Article › peer-review

Abstract

The extracellular matrix (ECM) provides structural support by serving as a scaffold for cells, and as such the ECM maintains normal tissue homeostasis and mediates the repair response following injury. In response to myocardial infarction (MI), ECM expression is generally upregulated in the left ventricle (LV), which regulates LV remodeling by modulating scar formation. The ECM directly affects scar formation by regulating growth factor release and cell adhesion and indirectly affects scar formation by regulating the inflammatory, angiogenic, and fibroblast responses. This review summarizes the current literature on ECM expression patterns and fibroblast mechanisms in the myocardium, focusing on the ECM response to MI. In addition, we discuss future research areas that are needed to better understand the molecular mechanisms of ECM action, both in general and as a means to optimize infarct healing.

Original language	American English
Journal	Journal of Cardiovascular Translational Research
Volume	5
DOIs	https://doi.org/10.1007/s12265-012-9398-z
State	Published - Dec 1 2012
Externally published	Yes

Keywords

Cardiac myocytes
Cell-ECM communication
Extracellular matrix
Fibroblasts
Myocardial infarction
Proteomics

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title = "Extracellular Matrix and Fibroblast Communication Following Myocardial Infarction",

abstract = " The extracellular matrix (ECM) provides structural support by serving as a scaffold for cells, and as such the ECM maintains normal tissue homeostasis and mediates the repair response following injury. In response to myocardial infarction (MI), ECM expression is generally upregulated in the left ventricle (LV), which regulates LV remodeling by modulating scar formation. The ECM directly affects scar formation by regulating growth factor release and cell adhesion and indirectly affects scar formation by regulating the inflammatory, angiogenic, and fibroblast responses. This review summarizes the current literature on ECM expression patterns and fibroblast mechanisms in the myocardium, focusing on the ECM response to MI. In addition, we discuss future research areas that are needed to better understand the molecular mechanisms of ECM action, both in general and as a means to optimize infarct healing.",

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AU - Halade, Ganesh V.

AU - Lindsey, Merry L.

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N2 - The extracellular matrix (ECM) provides structural support by serving as a scaffold for cells, and as such the ECM maintains normal tissue homeostasis and mediates the repair response following injury. In response to myocardial infarction (MI), ECM expression is generally upregulated in the left ventricle (LV), which regulates LV remodeling by modulating scar formation. The ECM directly affects scar formation by regulating growth factor release and cell adhesion and indirectly affects scar formation by regulating the inflammatory, angiogenic, and fibroblast responses. This review summarizes the current literature on ECM expression patterns and fibroblast mechanisms in the myocardium, focusing on the ECM response to MI. In addition, we discuss future research areas that are needed to better understand the molecular mechanisms of ECM action, both in general and as a means to optimize infarct healing.

AB - The extracellular matrix (ECM) provides structural support by serving as a scaffold for cells, and as such the ECM maintains normal tissue homeostasis and mediates the repair response following injury. In response to myocardial infarction (MI), ECM expression is generally upregulated in the left ventricle (LV), which regulates LV remodeling by modulating scar formation. The ECM directly affects scar formation by regulating growth factor release and cell adhesion and indirectly affects scar formation by regulating the inflammatory, angiogenic, and fibroblast responses. This review summarizes the current literature on ECM expression patterns and fibroblast mechanisms in the myocardium, focusing on the ECM response to MI. In addition, we discuss future research areas that are needed to better understand the molecular mechanisms of ECM action, both in general and as a means to optimize infarct healing.

KW - Cardiac myocytes

KW - Cell-ECM communication

KW - Extracellular matrix

KW - Fibroblasts

KW - Myocardial infarction

KW - Proteomics

UR - https://digitalcommons.usf.edu/intmed_facpub/61

U2 - 10.1007/s12265-012-9398-z

DO - 10.1007/s12265-012-9398-z

M3 - Article

VL - 5

JO - Journal of Cardiovascular Translational Research

JF - Journal of Cardiovascular Translational Research

ER -

Extracellular Matrix and Fibroblast Communication Following Myocardial Infarction

Abstract

Keywords

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