Dynamics of cardiac wound healing following myocardial infarction: Observations in genetically altered mice

W. M. Blankesteijn; E. Creemers; E. Lutgens; J. P.M. Cleutjens; M. J.A.P. Daemen; J. F.M. Smits

doi:10.1046/j.1365-201X.2001.00887.x

Dynamics of cardiac wound healing following myocardial infarction: Observations in genetically altered mice

W. M. Blankesteijn, E. Creemers, E. Lutgens, J. P.M. Cleutjens, M. J.A.P. Daemen, J. F.M. Smits

Cardiovascular Medicine

Research output: Contribution to journal › Review article › peer-review

Abstract

Recent improvements in the clinical management of acute myocardial infarction (MI) have resulted in a dramatic decrease in mortality because of this condition. This implies that more patients enter the process of infarct healing. This is a highly complex cascade of events which, although studied for decades, is still not completely understood. An increasing number of genetically altered mice can now be studied in a mouse model of MI, to investigate the contribution of the product of the targeted gene to the infarct healing process. In this review, we will discuss the defects in infarct healing that have been observed in null mutants for plasminogen, urokinase-type plasminogen activator (u-PA), matrix metalloproteinases (MMPS), thrombospondin-2 and dishevelled-1. These studies provide new insights in the infarct healing process itself, but may also help to define new diagnostic and therapeutic targets in humans suffering from MI.

Original language	English (US)
Pages (from-to)	75-82
Number of pages	8
Journal	Acta Physiologica Scandinavica
Volume	173
Issue number	1
DOIs	https://doi.org/10.1046/j.1365-201X.2001.00887.x
State	Published - 2001

Keywords

Dishevelled
Frizzled
Infarct rupture
Myocardial infarction
Plasminogen
Urokinase-type plasminogen activator
Wound healing

ASJC Scopus subject areas

Physiology

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10.1046/j.1365-201X.2001.00887.x

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title = "Dynamics of cardiac wound healing following myocardial infarction: Observations in genetically altered mice",

abstract = "Recent improvements in the clinical management of acute myocardial infarction (MI) have resulted in a dramatic decrease in mortality because of this condition. This implies that more patients enter the process of infarct healing. This is a highly complex cascade of events which, although studied for decades, is still not completely understood. An increasing number of genetically altered mice can now be studied in a mouse model of MI, to investigate the contribution of the product of the targeted gene to the infarct healing process. In this review, we will discuss the defects in infarct healing that have been observed in null mutants for plasminogen, urokinase-type plasminogen activator (u-PA), matrix metalloproteinases (MMPS), thrombospondin-2 and dishevelled-1. These studies provide new insights in the infarct healing process itself, but may also help to define new diagnostic and therapeutic targets in humans suffering from MI.",

keywords = "Dishevelled, Frizzled, Infarct rupture, Myocardial infarction, Plasminogen, Urokinase-type plasminogen activator, Wound healing",

author = "Blankesteijn, {W. M.} and E. Creemers and E. Lutgens and Cleutjens, {J. P.M.} and Daemen, {M. J.A.P.} and Smits, {J. F.M.}",

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T2 - Observations in genetically altered mice

AU - Blankesteijn, W. M.

AU - Creemers, E.

AU - Lutgens, E.

AU - Cleutjens, J. P.M.

AU - Daemen, M. J.A.P.

AU - Smits, J. F.M.

PY - 2001

Y1 - 2001

N2 - Recent improvements in the clinical management of acute myocardial infarction (MI) have resulted in a dramatic decrease in mortality because of this condition. This implies that more patients enter the process of infarct healing. This is a highly complex cascade of events which, although studied for decades, is still not completely understood. An increasing number of genetically altered mice can now be studied in a mouse model of MI, to investigate the contribution of the product of the targeted gene to the infarct healing process. In this review, we will discuss the defects in infarct healing that have been observed in null mutants for plasminogen, urokinase-type plasminogen activator (u-PA), matrix metalloproteinases (MMPS), thrombospondin-2 and dishevelled-1. These studies provide new insights in the infarct healing process itself, but may also help to define new diagnostic and therapeutic targets in humans suffering from MI.

AB - Recent improvements in the clinical management of acute myocardial infarction (MI) have resulted in a dramatic decrease in mortality because of this condition. This implies that more patients enter the process of infarct healing. This is a highly complex cascade of events which, although studied for decades, is still not completely understood. An increasing number of genetically altered mice can now be studied in a mouse model of MI, to investigate the contribution of the product of the targeted gene to the infarct healing process. In this review, we will discuss the defects in infarct healing that have been observed in null mutants for plasminogen, urokinase-type plasminogen activator (u-PA), matrix metalloproteinases (MMPS), thrombospondin-2 and dishevelled-1. These studies provide new insights in the infarct healing process itself, but may also help to define new diagnostic and therapeutic targets in humans suffering from MI.

KW - Dishevelled

KW - Frizzled

KW - Infarct rupture

KW - Myocardial infarction

KW - Plasminogen

KW - Urokinase-type plasminogen activator

KW - Wound healing

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Dynamics of cardiac wound healing following myocardial infarction: Observations in genetically altered mice

Abstract

Keywords

ASJC Scopus subject areas

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