ArticleJournal of the American Heart Association2023
Role of PARP and TRPM2 in VEGF Inhibitor-Induced Vascular Dysfunction.
Article in Journal of the American Heart Association, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Efficacy and safety of PARP inhibitors monotherapy or combination therapy with anti-angiogenics in ovarian cancer: a network meta-analysis.Frontiers in oncology · 2025Pooled it
- ROS-ATM-CBP axis-mediated PARP1 lactylation aggravates doxorubicin-induced cardiotoxicity.Clinical and translational medicine · 2026Article
- VEGF inhibitor-induced vascular dysfunction involves redox-sensitive PARP activation and SIRT1 disruption.Experimental physiology · 2026Article
- Vascular Protection of Poly(ADP-ribose) Polymerase Inhibitors in the Combination Therapy With Vascular Endothelial Growth Factor Signaling Pathway Inhibitors.Reviews in cardiovascular medicine · 2026Review
- PARPi Combining Nanoparticle LIN28B siRNA for the Management of Malignant Ascites.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Pathophysiological significance of the TRPM2 ion channel as a potential target in cancer, neurological disorders, and ischemia/reperfusion injury.Pharmacological research · 2026Review
- Salt-Induced Vascular Damage in Hypertension Involves Redox Activation of PARP/TRPM2 Signaling and Inflammasome Assembly.American journal of hypertension · 2025Article
- Revealing the Potential of Solamargine for Anti Metastasis and Angiogenesis Inhibition in Nasopharyngeal Carcinoma.Journal of inflammation research · 2025Article
- Article
- Role of transient receptor potential channels in the regulation of vascular tone.Drug discovery today · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Background Hypertension and vascular toxicity are major unwanted side effects of antiangiogenic drugs, such as vascular endothelial growth factor inhibitors (VEGFis), which are effective anticancer drugs but have unwanted side effects, including vascular toxicity and hypertension. Poly (ADP-ribose) polymerase (PARP) inhibitors, used to treat ovarian and other cancers, have also been associated with elevated blood pressure. However, when patients with cancer receive both olaparib, a PARP inhibitor, and VEGFi, the risk of blood pressure elevation is reduced. Underlying molecular mechanisms are unclear, but PARP-regulated transient receptor potential cation channel, subfamily M, member 2 (TRPM2), a redox-sensitive calcium channel, may be important. We investigated whether PARP/TRPM2 plays a role in VEGFi-induced vascular dysfunction and whether PARP inhibition ameliorates the vasculopathy associated with VEGF inhibition. Methods and Results Human vascular smooth muscle cells (VSMCs), human aortic endothelial cells, and wild-type mouse mesenteric arteries were studied. Cells/arteries were exposed to axitinib (VEGFi) alone and in combination with olaparib. Reactive oxygen species production, Ca
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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.