Local production of tenascin-C acts as a trigger for monocyte/macrophage recruitment that provokes cardiac dysfunction

ConclusionsBy promoting a pro-inflammatory microenvironment and macrophage migration, TNC appears to be a key factor to enable the MO/M Φ accumulation within fibrotic hearts leading to cardiac dysfunction. As TNC is highly expressed during inflammation and sparsely during the steady state, its inhibition could be a promising therapeutic strategy to control inflammation and immune cell infiltration in heart disease.
Source: Cardiovascular Research - Category: Cardiology Source Type: research