Osteopontin: Role in Extracellular Matrix Deposition and Myocardial Remodeling Post-MI

Mahipal Singh; Cerrone R. Foster; Suman Dalal; Krishna Singh

doi:10.1016/j.yjmcc.2009.06.015

Osteopontin: Role in Extracellular Matrix Deposition and Myocardial Remodeling Post-MI

Mahipal Singh, Cerrone R. Foster, Suman Dalal, Krishna Singh

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

Abstract

Remodeling after myocardial infarction (MI) associates with left ventricular (LV) dilation, decreased cardiac function and increased mortality. The dynamic synthesis and breakdown of extracellular matrix (ECM) proteins play a significant role in myocardial remodeling post-MI. Expression of osteopontin (OPN) increases in the heart post-MI. Evidence has been provided that lack of OPN induces LV dilation which associates with decreased collagen synthesis and deposition. Inhibition of matrix metalloproteinases, key players in ECM remodeling process post-MI, increased ECM deposition (fibrosis) and improved LV function in mice lacking OPN after MI. This review summarizes — 1) signaling pathways leading to increased expression of OPN in the heart; 2) the alterations in the structure and function of the heart post-MI in mice lacking OPN; and 3) mechanisms involved in OPN-mediated ECM remodeling post-MI.

Original language	American English
Journal	Journal of Molecular and Cellular Cardiology
Volume	48
DOIs	https://doi.org/10.1016/j.yjmcc.2009.06.015
State	Published - Mar 1 2010

Keywords

ECM
MMPs
myocardial infarction
myocardial remodeling
osteopontin

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Osteopontin Role in Extracellular Matrix Deposition and MyocardiFinal published version, 709 KBLicense: CC BY
Osteopontin Role in Extracellular Matrix Deposition and MyocardiFinal published version, 709 KBLicense: CC BY
Osteopontin Role in Extracellular Matrix Deposition and MyocardiFinal published version, 709 KBLicense: CC BY

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@article{26830cf345fc40baad6402d348c4f934,

title = "Osteopontin: Role in Extracellular Matrix Deposition and Myocardial Remodeling Post-MI",

abstract = " Remodeling after myocardial infarction (MI) associates with left ventricular (LV) dilation, decreased cardiac function and increased mortality. The dynamic synthesis and breakdown of extracellular matrix (ECM) proteins play a significant role in myocardial remodeling post-MI. Expression of osteopontin (OPN) increases in the heart post-MI. Evidence has been provided that lack of OPN induces LV dilation which associates with decreased collagen synthesis and deposition. Inhibition of matrix metalloproteinases, key players in ECM remodeling process post-MI, increased ECM deposition (fibrosis) and improved LV function in mice lacking OPN after MI. This review summarizes — 1) signaling pathways leading to increased expression of OPN in the heart; 2) the alterations in the structure and function of the heart post-MI in mice lacking OPN; and 3) mechanisms involved in OPN-mediated ECM remodeling post-MI.",

keywords = "ECM, MMPs, myocardial infarction, myocardial remodeling, osteopontin",

author = "Mahipal Singh and Foster, \{Cerrone R.\} and Suman Dalal and Krishna Singh",

year = "2010",

month = mar,

day = "1",

doi = "10.1016/j.yjmcc.2009.06.015",

language = "American English",

volume = "48",

journal = "Journal of Molecular and Cellular Cardiology",

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TY - JOUR

T1 - Osteopontin: Role in Extracellular Matrix Deposition and Myocardial Remodeling Post-MI

AU - Singh, Mahipal

AU - Foster, Cerrone R.

AU - Dalal, Suman

AU - Singh, Krishna

PY - 2010/3/1

Y1 - 2010/3/1

N2 - Remodeling after myocardial infarction (MI) associates with left ventricular (LV) dilation, decreased cardiac function and increased mortality. The dynamic synthesis and breakdown of extracellular matrix (ECM) proteins play a significant role in myocardial remodeling post-MI. Expression of osteopontin (OPN) increases in the heart post-MI. Evidence has been provided that lack of OPN induces LV dilation which associates with decreased collagen synthesis and deposition. Inhibition of matrix metalloproteinases, key players in ECM remodeling process post-MI, increased ECM deposition (fibrosis) and improved LV function in mice lacking OPN after MI. This review summarizes — 1) signaling pathways leading to increased expression of OPN in the heart; 2) the alterations in the structure and function of the heart post-MI in mice lacking OPN; and 3) mechanisms involved in OPN-mediated ECM remodeling post-MI.

AB - Remodeling after myocardial infarction (MI) associates with left ventricular (LV) dilation, decreased cardiac function and increased mortality. The dynamic synthesis and breakdown of extracellular matrix (ECM) proteins play a significant role in myocardial remodeling post-MI. Expression of osteopontin (OPN) increases in the heart post-MI. Evidence has been provided that lack of OPN induces LV dilation which associates with decreased collagen synthesis and deposition. Inhibition of matrix metalloproteinases, key players in ECM remodeling process post-MI, increased ECM deposition (fibrosis) and improved LV function in mice lacking OPN after MI. This review summarizes — 1) signaling pathways leading to increased expression of OPN in the heart; 2) the alterations in the structure and function of the heart post-MI in mice lacking OPN; and 3) mechanisms involved in OPN-mediated ECM remodeling post-MI.

KW - ECM

KW - MMPs

KW - myocardial infarction

KW - myocardial remodeling

KW - osteopontin

UR - https://dc.etsu.edu/etsu-works/8576

U2 - 10.1016/j.yjmcc.2009.06.015

DO - 10.1016/j.yjmcc.2009.06.015

M3 - Article

VL - 48

JO - Journal of Molecular and Cellular Cardiology

JF - Journal of Molecular and Cellular Cardiology

ER -

Osteopontin: Role in Extracellular Matrix Deposition and Myocardial Remodeling Post-MI

Abstract

Keywords

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