Wm. Blankesteijn et al., Dynamics of cardiac wound healing following myocardial infarction: observations in genetically altered mice, ACT PHYSL S, 173(1), 2001, pp. 75-82
Recent improvements in the clinical management of acute myocardial infarcti
on (MI) have resulted in a dramatic decrease in mortality because of this c
ondition. This implies that more patients enter the process of infarct heal
ing. This is a highly complex cascade of events which, although studied for
decades, is still not completely understood. An increasing number of genet
ically altered mice can now be studied in a mouse model of MI, to investiga
te the contribution of the product of the targeted gene to the infarct heal
ing process. In this review, we will discuss the defects in infarct healing
that have been observed in null mutants for plasminogen, urokinase-type pl
asminogen activator (u-PA), matrix metalloproteinases (MMPS), thrombospondi
n-2 and dishevelled-1. These studies provide new insights in the infarct he
aling process itself, but may also help to define new diagnostic and therap
eutic targets in humans suffering from MI.