ArticleExperimental biology and medicine (Maywood, N.J.)2020
Inhibition of protein kinase C beta phosphorylation activates nuclear factor-kappa B and improves postischemic recovery in type 1 diabetes.
Article in Experimental biology and medicine (Maywood, N.J.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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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
8 citing papers in PubMed.
- Short-Term: Cellular Metabolism and Gene Expression During the Onset of Diabetic Kidney Disease: A Diabetes Mellitus Experimental Model.International journal of molecular sciences · 2025Article
- Protein kinase C and endothelial dysfunction in select vascular diseases.Frontiers in cardiovascular medicine · 2025Review
- Network-based cytokine inference implicates Oncostatin M as a driver of an inflammation phenotype in knee osteoarthritis.Aging cell · 2024Article
- Novel components in the nuclear factor-kappa B (NF-κB) signaling pathways of endothelial cells under hyperglycemic-ischemic conditions.Frontiers in cardiovascular medicine · 2024Article
- Diabetes mellitus in peripheral artery disease: Beyond a risk factor.Frontiers in cardiovascular medicine · 2023Review
- Review
- ETS proto-oncogene 1 modulates PTP1B expression to participate in high glucose-mediated endothelial inflammation.Acta biochimica et biophysica Sinica · 2022Article
- Diabetes and Its Cardiovascular Complications: Comprehensive Network and Systematic Analyses.Frontiers in cardiovascular medicine · 2022Review
Corrections and comments
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Authors and funding
4 authors.
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Abstract
impact statementDiabetes worsens the outcomes of peripheral arterial disease (PAD) likely in part through inducing chronic inflammation. However, in PAD, recovery requires the nuclear factor-kappa B (NF-κB) activation, a known contributor to inflammation. Our study shows that individually, both ischemia and high glucose activate the canonical and non-canonical arms of the NF-κB pathways. We show for the first time that prolonged high glucose specifically impairs ischemia-induced activation of the canonical NF-κB pathway through activation of protein kinase C beta (PKCβ). Accordingly, inhibition of PKCβ restores the ischemia-induced NF-κB activity both
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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 Socratic graph.