ArticleThe Journal of biological chemistry2020
Inhibition of mitochondrial oxidative metabolism attenuates EMCV replication and protects β-cells from virally mediated lysis.
Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed.
- Interleukin-1 mediates innate immune signaling and antiviral defense in islets.Life science alliance · 2026Article
- Article
- Role of SIRT3 in the regulation of Gadd45α expression and DNA repair in β-cells.The Journal of biological chemistry · 2025Article
- Defining Cytokine Responsive and Non-responsive Human β-cells.Function (Oxford, England) · 2024Article
- Single Cell RNAseq Analysis of Cytokine-Treated Human Islets: Association of Cellular Stress with Impaired Cytokine Responsiveness.Function (Oxford, England) · 2024Article
- β-Cell-selective regulation of gene expression by nitric oxide.American journal of physiology. Regulatory, integrative and comparative physiology · 2024Article
- Cytokine and Nitric Oxide-Dependent Gene Regulation in Islet Endocrine and Nonendocrine Cells.Function (Oxford, England) · 2022Article
- Single-cell RNA sequencing of mouse islets exposed to proinflammatory cytokines.Life science alliance · 2021Article
- Inhibition of oxidative metabolism by nitric oxide restricts EMCV replication selectively in pancreatic beta-cells.The Journal of biological chemistry · 2020Article
- Regulation of ATR-dependent DNA damage response by nitric oxide.The Journal of biological chemistryArticle
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Viral infection is one environmental factor that may contribute to the initiation of pancreatic β-cell destruction during the development of autoimmune diabetes. Picornaviruses, such as encephalomyocarditis virus (EMCV), induce a pro-inflammatory response in islets leading to local production of cytokines, such as IL-1, by resident islet leukocytes. Furthermore, IL-1 is known to stimulate β-cell expression of iNOS and production of the free radical nitric oxide. The purpose of this study was to determine whether nitric oxide contributes to the β-cell response to viral infection. We show that nitric oxide protects β-cells against virally mediated lysis by limiting EMCV replication. This protection requires low micromolar, or iNOS-derived, levels of nitric oxide. At these concentrations nitric oxide inhibits the Krebs enzyme aconitase and complex IV of the electron transport chain. Like nitric oxide, pharmacological inhibition of mitochondrial oxidative metabolism attenuates EMCV-mediated β-cell lysis by inhibiting viral replication. These findings provide novel evidence that cytokine signaling in β-cells functions to limit viral replication and subsequent β-cell lysis by attenuating mitochondrial oxidative metabolism in a nitric oxide-dependent manner.
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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 OpenQuestion graph.