Nicotine-induced pulmonary artery smooth muscle cell dedifferentiation is facilitated by Cx43 phosphorylation at Ser368, driving pulmonary vascular remodeling.
Does nicotine induce pulmonary arterial remodeling via Cx43 phosphorylation at Ser368 in PASMCs?
Nicotine promotes pulmonary arterial remodeling through Cx43 phosphorylation at Ser368, identifying a potential therapeutic target for nicotine-related pulmonary vascular diseases.
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BACKGROUND: Pulmonary arterial hypertension is a severe disease characterized by pulmonary vascular remodeling, which is closely associated with the phenotypic switching of pulmonary artery smooth muscle cells (PASMCs). Connexin 43 (Cx43) phosphorylation is a key regulator of intercellular communication. However, the specific mechanism underlying nicotine-induced dedifferentiation of PASMCs remains unclear. PURPOSE: This study aimed to investigate the molecular mechanism by which Cx43 phosphorylation promotes nicotine-induced phenotypic switching of PASMCs, thereby driving pulmonary vascular remodeling. METHODS: Using Tagln-Cre; Cx43 RESULTS: Nicotine increased PASMC dedifferentiation by promoting Cx43 phosphorylation at Ser368 (Cx43-pS368). In Tagln-Cre; Cx43 CONCLUSION: Nicotine can induce PASMC phenotypic transformation by modulating Cx43-pS368, thereby promoting pulmonary artery remodeling. Targeting this pathway could provide a therapeutic strategy for nicotine-related pulmonary vascular diseases.
Xu et al. (Tue,) reported a other. Nicotine-induced pulmonary artery smooth muscle cell dedifferentiation is facilitated by Cx43 phosphorylation at Ser368, driving pulmonary vascular remodeling.
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