ArticleMolecular medicine (Cambridge, Mass.)2024
USF1 transcriptionally activates USP14 to drive atherosclerosis by promoting EndMT through NLRC5/Smad2/3 axis.
Article in Molecular medicine (Cambridge, Mass.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Deubiquitinases as Regulators and Therapeutic Targets in Vascular Diseases.International journal of molecular sciences · 2026Review
- USF1 transcriptionally activates TRIM55 to promote diabetic cardiomyopathy progression by enhancing HSPB1 protein degradation.Journal of bioenergetics and biomembranes · 2026Article
- Cellular Signalling Networks in High Altitude Pulmonary Hypertension: From Canonical Pathways to Emerging Targets.Cell proliferation · 2026Review
- USP7 Drives Atherosclerosis by Promoting Ferroptosis in Vascular Endothelial Cells via the KIAA1429/NEAT1/CTCF Axis.Biological procedures online · 2026Article
- Vascular smooth muscle cell RNA-binding protein U2AF2 induces copper death by regulating C1qbp expression, delaying development of atherosclerosise.Biological research · 2026Article
- Diabetes and its complications: molecular mechanisms, prevention and treatment.Signal transduction and targeted therapy · 2026Review
- Targeting PANoptosis in atherosclerosis: bridging cell death mechanisms and therapy.Apoptosis : an international journal on programmed cell death · 2026Review
- Endothelial-to-mesenchymal transition in the central nervous system: A potential therapeutic target to combat age-related vascular fragility.The Journal of pharmacology and experimental therapeutics · 2025Review
- USP7 Stabilizes USF1 to Aggravate ox-LDL-Induced Endothelial Injury Through the MYD88/NF-κB Pathway in Atherosclerosis.Applied biochemistry and biotechnology · 2025Article
- Recombinant chromosome 6 open reading frame 120 protein promotes angiogenesis and endothelial‑to‑mesenchymal transition in human umbilical vein endothelial cells via the PI3K/Akt signaling pathway.Molecular medicine reports · 2025Article
- Identification and validation of USP15 and CUL2 as ubiquitination related biomarker in chronic obstructive pulmonary disease.Hereditas · 2025Article
- New insights into the structure domain and function of NLR family CARD domain containing 5.Cell communication and signaling : CCS · 2025Review
- The role of deubiquitinases in cardiovascular diseases: mechanisms and therapeutic implications.Frontiers in cardiovascular medicine · 2025Review
- Hydroxysafflor yellow A, a natural food pigment, ameliorates atherosclerosis in ApoEFood science & nutrition · 2024Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundEndothelial-to-Mesenchymal Transformation (EndMT) plays key roles in endothelial dysfunction during the pathological progression of atherosclerosis; however, its detailed mechanism remains unclear. Herein, we explored the biological function and mechanisms of upstream stimulating factor 1 (USF1) in EndMT during atherosclerosis.
methodsThe in vivo and in vitro atherosclerotic models were established in high fat diet-fed ApoE
resultsUSF1 was up-regulated in atherosclerosis patients. USF1 knockdown inhibited EndMT by up-regulating CD31 and VE-Cadherin, while down-regulating α-SMA and vimentin, thereby repressing inflammation, and migration in ox-LDL-exposed HUVECs. In addition, USF1 transcriptionally activated ubiquitin-specific protease 14 (USP14), which promoted de-ubiquitination and up-regulation of NLR Family CARD Domain Containing 5 (NLRC5) and subsequent Smad2/3 pathway activation. The inhibitory effect of sh-USF1 or sh-USP14 on EndMT was partly reversed by USP14 or NLRC5 overexpression. Finally, USF1 knockdown delayed atherosclerosis progression via inhibiting EndMT in mice.
conclusionOur findings indicate the contribution of the USF1/USP14/NLRC5 axis to atherosclerosis development via promoting EndMT, which provide effective therapeutic targets.
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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 OpenQuestion graph.