ArticleFrontiers in pharmacology2022
Pharmacological inhibition of protein tyrosine kinases axl and fyn reduces TNF-α-induced endothelial inflammatory activation
Article in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Article
- Ultrasound molecular imaging in evaluating the severity of ischemia-reperfusion injury-induced acute kidney injury.Quantitative imaging in medicine and surgery · 2025Article
- The Vulnerable Vascular Network: Endothelial Dysfunction as a Central Driver of Intestinal Inflammation-A Systematic Review.Biomedicines · 2025Review
- Targeting synergetic endothelial inflammation by inhibiting NFKB and JAK-STAT pathways.iScience · 2025Article
- Ultrasound molecular imaging for early detection of acute renal ischemia-reperfusion injury.Bioengineering & translational medicine · 2024Article
- Review
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Major surgery induces systemic inflammation leading to pro-inflammatory activation of endothelial cells. Endothelial inflammation is one of the drivers of postoperative organ damage, including acute kidney injury Tumour Necrosis Factor alpha (TNF-α) is an important component of surgery-induced pro-inflammatory activation of endothelial cells. Kinases, the backbone of signalling cascades, can be targeted by pharmacological inhibition. This is a promising treatment option to interfere with excessive endothelial inflammation. In this study, we identified activated kinases as potential therapeutic targets. These targets were pharmacologically inhibited to reduce TNF-α-induced pro-inflammatory signalling in endothelial cells. Kinome profiling using PamChip arrays identified 64 protein tyrosine kinases and 88 serine-threonine kinases, the activity of which was determined at various timepoints (5-240 min) following stimulation with 10 ng/ml TNF-α in Human umbilical vein endothelial cells
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