Commentary Free access Phone: Find articles by Chen, Y. Find articles by Cao, Y. Published October 15, - More info. In recent decades, treatments for myocardial infarction MI , such as stem and progenitor cell therapy, have attracted considerable scientific and clinical attention but failed to improve patient outcomes.
These efforts indicate that more rigorous mechanistic and functional testing of potential MI therapies is required. However, the mechanisms underlying this proposed therapeutic approach remain vague and untested.
The results obtained using all 3 genetic approaches were highly concordant and demonstrated that loss of lymphatic vessel growth did not impair left ventricular ejection fraction 2 weeks after MI in mice. We observed a trend toward excess fluid in the infarcted region of the left ventricle, but immune cell infiltration and clearance were unchanged with loss of expanded lymphatics.
These studies refute the hypothesis that lymphangiogenesis contributes significantly to cardiac function after MI, and suggest that any effect of exogenous VEGF-C is likely to be mediated by nonlymphangiogenic mechanisms. Tang, Carl Wittig, Andrea A. Guerrero, Stephanie Sterling, N. Gimotty, Mark L. Cardiac lymphatics have emerged as a therapeutic target in cardiovascular diseases to limit myocardial edema and inflammation, notably after myocardial infarction MI.
While most experimental therapeutic approaches have focused on vascular endothelial growth factor C VEGF-C delivery, it remains uncertain to what degree the beneficial cardiac effects are related to lymphatic expansion in the heart. Their data, obtained by elegant comparisons of several complementary genetic mouse models, indicate that infarct expansion and left ventricular dilation and function after MI are unaffected by infarct lymphangiogenesis.
