ArticleMolecular medicine reports2017
High expression of ubiquitin-specific peptidase 39 is associated with the development of vascular remodeling.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- USP39 promotes retinal pathological angiogenesis in retinopathy of prematurity by stabilizing SIRT2 expression through deubiquitination.International ophthalmology · 2025Article
- USP39: a key regulator in malignant tumor progression.Frontiers in oncology · 2025Review
- USP39 at the crossroads of cancer immunity: regulating immune evasion and immunotherapy response through RNA splicing and ubiquitin signaling.Frontiers in immunology · 2025Review
- Endothelial deubiquinatase YOD1 mediates Ang II-induced vascular endothelial-mesenchymal transition and remodeling by regulating β-catenin.Acta pharmacologica Sinica · 2024Article
- The Role of Deubiquitinases in Vascular Diseases.Journal of cardiovascular translational research · 2020Review
- USP39 regulates the cell cycle, survival, and growth of human leukemia cells.Bioscience reports · 2019Article
Corrections and comments
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Authors and funding
6 authors.
Funding
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Abstract
Vascular remodeling is the primary cause underlying the failure of angioplasty surgeries, including vascular stenting, transplant vasculopathy and vein grafts. Multiple restenosis‑associated proteins and genes have been identified to account for this. In the present study, the functions of ubiquitin‑specific peptidase 39 (USP39) were investigated in the context of two vascular remodeling models (a mouse common carotid artery ligation and a pig bilateral saphenous vein‑carotid artery interposition graft). USP39 has previously been observed to be upregulated in ligated arteries, and this result was confirmed in the pig vein graft model. In addition, Transwell assay results demonstrated that vascular smooth muscle cell (VSMC) migration was suppressed by lentiviral vector‑mediated downregulation of USP39 and enhanced by upregulation of USP39. Furthermore, knockdown of USP39 inhibited VSMC cell proliferation and the expression of cyclin D1 and cyclin‑dependent kinase 4, as analyzed via cell counting, MTT assay and western blotting. These results suggest that USP39 may represent a novel therapeutic target for treating vascular injury and preventing vein-graft failure.
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