ArticleAmerican journal of physiology. Cell physiology2025
Oxidized phosphatidylcholines activate NOX1-mediated oxidative stress response and shift glucose metabolism in cardiac cells.
Article in American journal of physiology. Cell physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- ML-171 Attenuates Pentylenetetrazole-Associated Oxidative and Apoptotic Injury Without Robust Suppression of Seizure Expression: An In Vitro and In Vivo Study.International journal of molecular sciences · 2026Article
- NOX2 exacerbates periodontitis via JAK2-STAT3-mediated ferroptosis of gingival epithelial cells.Frontiers in immunology · 2026Article
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8 authors.
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Abstract
In cardiometabolic syndrome, the development of cardiovascular disease is linked with an increase in systemic oxidative stress. The formation of free radical species leads to the oxidative modification of lipids, including oxidized phosphatidylcholines (OxPCs), which have been implicated in the progression of cardiovascular diseases in humans. We found that reducing plasma levels of OxPCs in mice by adeno-associated virus (AAV)-mediated hepatic expression of an OxPC-targeting antibody fragment (scFv-E06) resulted in significant transcriptional changes in the heart, particularly affecting genes involved in metabolism, redox processes, and fibrosis. To investigate the response of cardiac myoblasts to OxPCs in vitro, we exposed H9c2 cells to a defined mixture of OxPC species [oxidized 1-palmitoyl-2-arachidonoyl-
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