ArticleDiabetes, metabolic syndrome and obesity : targets and therapy2022
Loss of OTUD6B Stimulates Angiogenesis and Promotes Diabetic Atherosclerosis.
Article in Diabetes, metabolic syndrome and obesity : targets and therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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
2 citing papers in PubMed, 2 citations in OpenAlex.
- Otud6b induces pulmonary arterial hypertension by mediating the Calpain-1/HIF-1α signaling pathway.Cellular and molecular life sciences : CMLS · 2024Article
- Potential new therapeutic targets: Association of microRNA with atherosclerotic plaque stability.International journal of immunopathology and pharmacologyReview
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Angiogenesis is an essential promoter of atherosclerotic plaque rupture. However, the mechanism of its regulation is not understood. OTUD6B regulates cell proliferation, migration, and angiogenesis. We investigated the role of OTUD6B in angiogenesis in diabetic atherosclerotic plaques. Patients and Methods: The expression of OTUD6B was analyzed by single cell RNA sequencing (scRNA-seq) and RNA sequencing (RNA-seq) and evaluated by Immunofluorescence in human anterior tibial arteries from diabetic amputees and ApoE Results: We found that OTUD6B expression was markedly downregulated in human anterior tibial arteries from diabetic amputees and ApoE Conclusion: OTUD6B can reduce angiogenesis in atherosclerotic plaques, enhance plaque stability and delay the progression of atherosclerosis by regulating the proliferation, migration, and lumen formation of endothelial cells.
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Registered trials
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