ArticleNaunyn-Schmiedeberg's archives of pharmacology2025
Cilostazol alleviates imatinib-induced myocardial injury in rats by modulating the TGF-β1/MAPK, SHC/Grb2/SOS signaling pathways and upregulating miRNA-195-5P.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 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.
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Who cites it
1 citing paper in PubMed, 1 synthesis or guideline pooled it.
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tyrosine kinase inhibitors have revolutionized cancer treatment, yet their association with cardiotoxicity remains a challenge. While the pathophysiological consequences of imatinib therapy involve diverse pathways, our understanding of these mechanisms is limited. Cilostazol, a selective phosphodiesterase 3 inhibitor used in intermittent claudication treatment, is known for its antioxidant and anti-inflammatory effects. In this study, we aimed to counteract the cardiotoxic effects of imatinib by administering cilostazol, concurrently investigating the precise mechanisms underlying imatinib-induced myocardial injury. Twenty-eight male Wistar rats were categorized into four groups: control (2 mL/kg normal saline, orally), cilostazol (10 mg/kg, orally), imatinib (40 mg/kg, intraperitonially), and combination (cilostazol and imatinib). Daily treatments were administered for 28 consecutive days. Imatinib therapy induced oxidative stress, pro-inflammatory responses, and cardiotoxicity biomarkers, alongside dysregulation of various protein and gene expressions. The addition of cilostazol to imatinib mitigated these deleterious effects, notably restoring measured biomarkers close to normal values. Histopathological investigations corroborated the biochemical findings. The co-administration of cilostazol with imatinib effectively protects against imatinib-induced myocardial injury in rats, reducing oxidative stress, apoptotic and inflammatory biomarkers, and modulating protein, gene, and miRNA-195-5p expression levels. While promising for alleviating and protecting against myocardial injury in imatinib-treated patients, these findings necessitate further confirmation through clinical studies.
Indexed as
Identifiers
40100370What Socratic holds
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.