Key result
This review summarizes literature data on the role of PKCd and ERK1/2 in mediating the mitogenic action of thrombin in vascular smooth muscle cells.
This review highlights the mechanistic roles of PKCd and ERK1/2 in thrombin-induced vascular smooth muscle cell proliferation, relevant to atherosclerosis and hypertension.
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Mechanistic data on PKCδ/ERK1/2 in thrombin-driven VSMC proliferation remain preclinical; leaves open therapeutic translation to atherosclerosis or hypertension.
Cardiovascular disease is the greatestest single cause of mortality and its major underlying pathology is atherosclerosis. The proliferation of vascular smooth muscle cells (VSMC) is a key event in the pathogenesis of various vascular diseases, including atherosclerosis and hypertension. Thrombin is involved in the differentiation and abnormal proliferation of VSMC associated with atherosclerosis and hypertension. Thrombin stimulation results in extracellular signal-regulated kinase (ERK1/2) activation through transactivation of the epidermal growth factor receptor (EGFR). Based on our reacent studies in which PD98059 used to inhibit ERK1/2, we have shown previously that ERK1/2 was involved in the regulation by thrombin of VSMC's proliferation. In addition, protein kinase C delta (PKCd) have also been detected in VSMC and shown to be regulated by thrombin. In this review, we are presenting literature data relating to role of PKCd and ERK1/2 in mediating the mitogenic action of thrombin in VSMC.
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Smiljanić et al. (2013) conducted a review in Atherosclerosis and hypertension. PKCd and ERK1/2 was evaluated on Mitogenic action of thrombin in vascular smooth muscle cells. This review summarizes literature data on the role of PKCd and ERK1/2 in mediating the mitogenic action of thrombin in vascular smooth muscle cells.
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