Abstract
Background and Aims: Besides the traditional role attributed to the cellular communication network factor 2 (CCN2/CTGF) as a main mediator of transforming growth factor β (TGF-β) induced fibrotic responses, recent evidences have demonstrated a direct role of CCN2 acting as a growth factor in vascular smooth muscle cells (VSMCs) inducing oxidative and proinflammatory responses. However, presence of both, CCN2 and TGF-β, are needed to induce a persistent fibrotic response in some tissues. Aims: Considering the main role of TGF-β receptors (TβR) in the TGF-β pathway activation, our aim was to explore the effects of CCN2 in the regulation of TβRI and TβRII levels in VSMCs.
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