ArticleJournal of bioenergetics and biomembranes2021
TRIM32 inhibits the proliferation and migration of pulmonary artery smooth muscle cells through the inactivation of PI3K/Akt pathway in pulmonary arterial hypertension.
Article in Journal of bioenergetics and biomembranes, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 24 citations in OpenAlex.
- Bellidifolin Improves Pulmonary Artery Smooth Muscle Cells Proliferation by Targeting the IGFBP5-Mediated PI3K-AKT-mTOR Pathway and Dilates the Pulmonary Artery.Biomolecules · 2026Article
- Emerging Role and Potential Therapeutic Application of TRIM Proteins in Cardiovascular Diseases.Biomolecules · 2026Review
- Emerging significance of E3 ubiquitin ligases and Deubiquitinases in pulmonary hypertension.Molecular medicine (Cambridge, Mass.) · 2026Review
- Mechanistic Investigation of Calcium Channel Regulation-Associated Genes in Pulmonary Arterial Hypertension and Signatures for Diagnosis.Molecular biotechnology · 2025Article
- New insights into the role of ubiquitination in angiogenesis (Review).International journal of molecular medicine · 2025Review
- Bioactive compound combinations fromFrontiers in pharmacology · 2025Article
- Beyond Tumors: The Pivotal Role of TRIM Proteins in Chronic Non-Tumor Lung Diseases.Journal of inflammation research · 2025Review
- The novel roles of YULINK in the migration, proliferation and glycolysis of pulmonary arterial smooth muscle cells: implications for pulmonary arterial hypertension.Biological research · 2023Article
- CoClFEBS open bio · 2023Article
- Interleukin-6 and pulmonary hypertension: from physiopathology to therapy.Frontiers in immunology · 2023Review
- Synemin promotes pulmonary artery smooth muscle cell phenotypic switch in shunt-induced pulmonary arterial hypertension.ESC heart failure · 2022Article
- The Potential Application and Promising Role of Targeted Therapy in Pulmonary Arterial Hypertension.Biomedicines · 2022Review
- [Tanshinone IIA alleviates monocrotaline-induced pulmonary hypertension in rats through the PI3K/Akt-eNOS signaling pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Article
- Inhibition of KIF23 Alleviates IPAH by Targeting Pyroptosis and Proliferation of PASMCs.International journal of molecular sciences · 2022Article
- Inhibition of TRIM32 by ibr-7 treatment sensitizes pancreatic cancer cells to gemcitabine via mTOR/p70S6K pathway.Journal of cellular and molecular medicine · 2022Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pulmonary arterial hypertension (PAH) is a progressive and fetal cardiovascular disease. Tripartite motif 32 (TRIM32) is a member of TRIM family that has been found to be involved in cardiovascular disease. However, the role of TRIM32 in PAH remains unclear. Here we investigated the effects of TRIM32 on hypoxia-induced pulmonary artery smooth muscle cells (PASMCs) in vitro. Our results showed that TRIM32 protein level in the plasma samples from PAH patients was decreased as compared with healthy volunteers. Exposure to hypoxia condition caused a significant decrease in TRIM32 expression in PASMCs. Overexpression of TRIM32 inhibited hypoxia-induced proliferation and migration of PASMCs. TRIM32 overexpression elevated the increased apoptotic rate and caspase-3 activity in hypoxia-induced PASMCs. Moreover, overexpression of TRIM32 reversed hypoxia-induced down-regulation of myocardin, SM 22 and calponin, as well as up-regulation of osteopontin (OPN). Whereas, TRIM32 knockdown shwed the opposite effect. Furthermore, overexpression of TRIM32 inhibited hypoxia-induced activation of PI3K/Akt with decreased phosphorylated level of PI3K and Akt. Additionally, activation of PI3K/Akt by IGF-1 treatment reversed the effects of TRIM32 on hypoxia-induced PASMCs. In conclusion, these findings indicated that TRIM32 was involved in the development of PAH through regulating the proliferation, migration, apoptosis and dedifferentiation of PASMCs, which might be mediated by the PI3K/Akt signaling pathway. Thus, TRIM32 might be a potential target for PAH treatment.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.