Endogenous IP-10 acts as an essential inhibitory signal that promotes wound contraction and attenuates adverse remodeling following myocardial infarction.
Endogenous IP-10 is an essential inhibitory signal that regulates the cellular composition of the healing infarct and promotes wound contraction, attenuating adverse remodeling. IP-10-mediated actions may be due, at least in part, to direct effects on fibroblast migration and function.
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Bujak et al. (2009) studied this question.
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