ArticleRSC advances2019
Knockdown of USP14 inhibits PDGF-BB-induced vascular smooth muscle cell dedifferentiation
Article in RSC advances, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- RICTOR Prevents Decidualization Disorder in Women With Advanced Maternal Age via Regulating FoxO1 Nuclear Export.Aging cell · 2026Article
- Bortezomib Suppresses Abnormal Proliferation, Migration, and Phenotypic Switching of Aortic Smooth Muscle Cells.Acta Cardiologica Sinica · 2026Article
- Neointimal hyperplasia and vascular restenosis: from molecular mechanisms to therapeutic interventions.Molecular biomedicine · 2026Review
- USP14 deficiency inhibits neointima formation following vascular injury via degradation of Skp2 protein.Cell death discovery · 2024Article
- USF1 transcriptionally activates USP14 to drive atherosclerosis by promoting EndMT through NLRC5/Smad2/3 axis.Molecular medicine (Cambridge, Mass.) · 2024Article
- Roles of ubiquitin-specific proteases in inflammatory diseases.Frontiers in immunology · 2024Review
- A role of TRIM59 in pulmonary hypertension: modulating the protein ubiquitylation modification.Journal of translational medicine · 2023Article
- Ubiquitin-Specific Proteases (USPs) and Metabolic Disorders.International journal of molecular sciences · 2023Review
- Mitophagy in atherosclerosis: from mechanism to therapy.Frontiers in immunology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerosis is a chronic progressive cardiovascular disease, which may result in many clinical consequences. Ubiquitin-specific protease 14 (USP14), a member of the USP family, has been found to be involved in cardiovascular disease. In the present study, we aimed to explore the role of USP14 in atherosclerosis. The results showed that USP14 expression was markedly increased in atherosclerotic tissues as compared to control tissues. Then we next examined the role of USP14 in primary human aortic smooth muscle cells (HASMCs) in response to PDGF-BB stimulation. The results demonstrated that PDGF-BB induced the USP14 expression in a dose- and time-dependent manner. Knockdown of USP14 in HASMCs suppressed PDGF-BB-induced proliferation and migration of HASMCs. The expressions of VSMCs markers including α-SMA, calponin and SM-MHC were markedly increased by knockdown of USP14, indicating that USP14 knockdown suppressed phenotypic modulation of HASMCs. However, USP14 overexpression exhibited the opposite effects. Furthermore, PDGF-BB-induced phosphorylation of mTOR and P70S6K in HASMCs was prevented by knockdown of USP14. In addition, MHY-1485, an activator of mTOR signaling, reversed the effects of USP14 knockdown on PDGF-BB-induced HASMCs. These data suggested that knockdown of USP14 prevented PDGF-BB-induced proliferation, migration, and phenotypic modulation of HASMCs
Identifiers
What OpenQuestion holds
Registered trials
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 OpenQuestion graph.