ArticleESC heart failure2022
Synemin promotes pulmonary artery smooth muscle cell phenotypic switch in shunt-induced pulmonary arterial hypertension.
Article in ESC heart failure, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Down syndrome child with multiple heart diseases: A case report.World journal of cardiology · 2023Article
- A year in heart failure: updates of clinical and preclinical findings.ESC heart failure · 2023Review
- Biology and function of pericytes in the vascular microcirculation.Animal models and experimental medicine · 2023Review
- Synemin promotes pulmonary artery smooth muscle cell phenotypic switch in shunt-induced pulmonary arterial hypertension.ESC heart failure · 2022Article
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsAlthough considerable progress has been made in the diagnosis and treatment of congenital heart disease-associated pulmonary heart hypertension (CHD-PAH), the clinical prognosis and overall survival of patients with CHD-PAH remain poor. Therefore, the molecular pathogenesis of CHD-PAH requires further investigation. The intermediate filament protein synemin (SYN) is reported to modulate phenotypic alterations and varicose vein development, but there is little understanding of its exact functions in CHD-PAH. METHODS AND
resultsSYN expression in the pulmonary arterioles of CHD-PAH patients and shunt-induced PAH rat models was evaluated using immunohistochemistry and western blot. Cell counts and Transwell migration assays were used to assess the effect of SYN on the proliferation and migration capability of human pulmonary smooth muscle cells (hPASMCs). Adeno-associated viruses (AAVs) have been used to suppress SYN expression in the pulmonary arterioles of rats. Such rats were further used to construct a shunt-induced PAH animal model to investigate the function of SYN in PAH and pulmonary vascular remodelling. Compared with the normal control group, SYN expression was found to be clearly up-regulated in the remodelled pulmonary arterioles of CHD-PAH and shunt-induced PAH rat models. In addition, SYN suppression increased the expression of hPASMC contractile-phenotype markers and decreased the expression of synthetic phenotype markers, in contrast to the control group. SYN suppression also dramatically attenuated the proliferation and migration capability of hPASMCs. Conversely, SYN overexpression promoted phenotypic switch, proliferation, and migration of hPASMCs, whereas these effects were notably alleviated by the protein kinase B (AKT) inhibitor MK-2206. Furthermore, we confirmed that SYN suppression mitigated PAH and pulmonary vascular remodelling induced by high blood flow in vivo.
conclusionsOur findings indicated that SYN may represent a promising therapeutic target in the treatment of CHD-PAH.
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