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Transmembrane protein 66 attenuates neointimal hyperplasia after carotid artery injury by SOCE inactivation
Molecular Medicine Reports
Neointimal hyperplasia could be one of the most important complications after balloon angioplasty. Since calcium signaling has several physiologic effects on the regulation of the proliferation and migration of vascular smooth muscle cells (VSMCs), it was hypothesized that transmembrane protein 66 (TMEM66), a store operated calcium entry (SOCE)‑associated regulatory factor, possesses vascular protection against balloon injury. The rat balloon‑induced carotid artery injury model was performed.doi:10.3892/mmr.2019.10328 pmid:31173198 fatcat:kci3zdfx6rautjdsyqnj4qoli4