Key result
Atorvastatin protected against PAH-induced increases in RVSP and vascular remodeling in rats, and inhibited proliferation while triggering apoptosis in hPASMCs.
Why the study?
To explore the role of atorvastatin in rescuing pulmonary artery hypertension by inhibiting the AKT/ERK-dependent PDGF-BB/HIF-1α axis.
Does atorvastatin improve pulmonary artery hypertension and inhibit vascular remodeling in preclinical models?
Does atorvastatin improve pulmonary artery hypertension and inhibit vascular remodeling in preclinical models?
Answers are grounded in this paper and cite their sources.
Atorvastatin attenuates pulmonary artery hypertension in preclinical models by inhibiting the AKT/ERK-dependent PDGF-BB/HIF-1α axis.
BACKGROUND: The aim of this study is to explore the role of atorvastatin in rescuing pulmonary artery hypertension (PAH) by inhibiting the AKT/ERK-dependent PDGF-BB/HIF-1α axis. METHODS: PAH model in rats was established by MCT induction, followed by Atorvastatin intervention. Pulmonary hemodynamic measurement and pulmonary morphological evaluation in rats were conducted. Human pulmonary artery smooth muscle cells (hPASMCs) were subjected to hypoxic exposure or PDGF-BB treatment, followed by atorvastatin induction. Relative levels of HIF-1α, p-ERK and p-Akt were detected. Viability and apoptosis were respectively determined by cell counting kit-8 (CCK-8) assay and flow cytometry. RESULTS: Atorvastatin protected PAH-induced increases in RVSP and Fulton's index in rats. Meanwhile, it inhibited vascular remodeling following PAH by downregulating HIF-1α and PDGF-BB. Hypoxia or PDGF-BB treatment in hPASMCs resulted in upregulation of p-ERK and p-Akt, and viability increase, which were partially abolished by Atorvastatin intervention. In addition, atorvastatin triggered apoptosis in hypoxia or PDGF-BB-induced hPASMCs. CONCLUSIONS: Atorvastatin inhibits the activation of HIF-1α and proliferative ability, and triggers apoptosis in hPASMCs exposed to hypoxia or PDGF-BB treatment through inactivating the AKT/ERK pathway.
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Chen et al. (2021) studied Pulmonary artery hypertension. Atorvastatin was evaluated on RVSP, Fulton's index, and vascular remodeling. Atorvastatin protected against PAH-induced increases in RVSP and vascular remodeling in rats, and inhibited proliferation while triggering apoptosis in hPASMCs.
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