Key result
CREB mediates transcriptional, proliferative, and migratory responses of Angiotensin II in vascular smooth muscle cells, playing a crucial role in vascular injury-induced neointimal growth.
This review highlights the critical role of CREB in mediating Ang II-induced vascular smooth muscle cell proliferation, hypertrophy, and migration, which are key processes in vascular remodeling and disease.
CREB targeting remains investigational; leaves open whether inhibition reduces clinical restenosis.
Cyclic AMP response element (CRE) binding protein (CREB) is a nuclear transcription factor that regulates the transcription of several genes containing the CRE sites on their promoters. CREB is activated by phosphorylation on a key serine residue, Ser311, in response to a wide variety of extracellular stimuli including angiotensin II (Ang II). Ang II is an important vasoactive peptide and mitogen for vascular smooth muscle cells (VSMC) that in addition to regulating the contractile response in VSMC also plays an important role in phenotypic switch of VSMC from contractile to a synthetic state. The synthetic VSMC are known to exhibit proliferative and migratory properties due to hyperactivation of Ang II-induced signaling events. Ang II has been shown to induce CREB phosphorylation/activation and transcription of genes implicated in proliferation, growth, and migration. Here, we have highlighted some key studies that have demonstrated an important role of CREB in Ang II-mediated gene transcription, proliferation, hypertrophy, and migration of VSMC.
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Truong et al. (2020) conducted a review in Vascular smooth muscle cell responses to Angiotensin II. Angiotensin II was evaluated. CREB mediates transcriptional, proliferative, and migratory responses of Angiotensin II in vascular smooth muscle cells, playing a crucial role in vascular injury-induced neointimal growth.
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