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Background : Hyperhomocysteinemia (HHcy) is an independent risk factor of cardiovascular diseases. Extracellular signal-regulated kinase-1/2 (ERK-1/2) and the JAK/STAT pathway kinase, signal transducer and activator of transcription 3 (STAT3), are involved in matrix metalloproteinase-9 (MMP-9) induction and matrix remodeling. However, their role in homocysteine (Hcy)-mediated MMP-9 induction and matrix remodeling is unclear. Clinical and experimental evidence indicates that HHcy and activation of the renin-angiotensin system, mediated by angiotensin II type 1 (AT1) receptor, are involved in a variety of vascular pathologies. Despite this fact, the relationship between HHcy and activation of the renin-angiotensin system has not been comprehensively characterized. Therefore, we hypothesized that Hcy activates AT1 receptor that potentiates STAT3 via ERK-1/2 phosphorylation. STAT3 modulates target MMP-9 and collagen, resulting in vascular remodeling.

Synergism between AT1 receptor and hyperhomocysteinemia during vascular remodeling