ReviewDrug design, development and therapy2024
Understanding Sorafenib-Induced Cardiovascular Toxicity: Mechanisms and Treatment Implications.
Review in Drug design, development and therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
23 citing papers in PubMed, 31 citations in OpenAlex.
- Article
- Article
- Cardiovascular Toxicity in Cancer Therapy: Potential Mechanisms of Ferroptosis and Treatment Strategies.Cells · 2026Review
- Integrating high-fidelity hiPSC-cardiomyocytes with AI-driven modeling for enhanced proarrhythmic risk assessment.Archives of toxicology · 2026Article
- Hypertension associated with systemic therapy for hepatocellular carcinoma and management strategies.Frontiers in pharmacology · 2026Review
- VESNA: an open-source tool for automated 3D vessel segmentation and network analysis.BMC bioinformatics · 2025Article
- Vitamin B17 alleviates Sorafenib-induced cardiotoxicity in Ehrlich Ascites Carcinoma mice via modulation of inflammatory and fibrotic pathways.Scientific reports · 2025Article
- EET-Based Therapeutics Mitigate Sorafenib-Associated Glomerular Cell Damage.Biomolecules · 2025Article
- Naringenin: A potential therapeutic agent for modulating angiogenesis and immune response in hepatocellular carcinoma.Journal of pharmaceutical analysis · 2025Article
- A pharmacovigilance study of thromboembolism events associated with vascular endothelial growth factor receptor tyrosine kinase inhibitors based on FAERS database.Scientific reports · 2025Article
- Identification and validation of prognostic models and tumor microenvironment infiltration characteristics for tRNA modification regulators in clear cell renal cell carcinoma.Oncology letters · 2025Article
- Oxocrebanine inhibits the proliferation of hepatocellular carcinoma cells by promoting apoptosis and autophagy.World journal of gastrointestinal oncology · 2025Article
- The Imaging Value ofMolecular imaging and biology · 2025Article
- Understanding the Mechanisms of Chemotherapy-Related Cardiotoxicity Employing hiPSC-Derived Cardiomyocyte Models for Drug Screening and the Identification of Genetic and Epigenetic Variants.International journal of molecular sciences · 2025Review
- Sorafenib-Drug Delivery Strategies in Primary Liver Cancer.Journal of functional biomaterials · 2025Review
- Cardiotoxicity of Chemotherapy: A Multi-OMIC Perspective.Journal of xenobiotics · 2025Review
- Folic Acid-Targeted Liposome-Based Nanoparticle Loaded with Sorafenib for Liver Cancer Therapy.International journal of nanomedicine · 2025Article
- Recurrent desmoid tumors with ureteric fistula: a case report and literature review.Frontiers in pediatrics · 2025Article
- Decoding Drug Interactions: Character and Degree of Pharmacokinetic Interactions Between Telmisartan and Sorafenib or Donafenib in Rats.Drug design, development and therapy · 2025Article
- Mechanisms of sorafenib-induced cardiotoxicity: ER stress induces upregulation of ATF3, leading to downregulation of NDUFS1 expression and mitochondrial dysfunction.Frontiers in pharmacology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tyrosine kinase inhibitors (TKIs) have been recognized as crucial agents for treating various tumors, and one of their key targets is the intracellular site of the vascular endothelial growth factor receptor (VEGFR). While TKIs have demonstrated their effectiveness in solid tumor patients and increased life expectancy, they can also lead to adverse cardiovascular effects including hypertension, thromboembolism, cardiac ischemia, and left ventricular dysfunction. Among the TKIs, sorafenib was the first approved agent and it exerts anti-tumor effects on hepatocellular carcinoma (HCC) and renal cell carcinoma (RCC) by inhibiting angiogenesis and tumor cell proliferation through targeting VEGFR and RAF. Unfortunately, the adverse cardiovascular effects caused by sorafenib not only affect solid tumor patients but also limit its application in curing other diseases. This review explores the mechanisms underlying sorafenib-induced cardiovascular adverse effects, including endothelial dysfunction, mitochondrial dysfunction, endoplasmic reticulum stress, dysregulated autophagy, and ferroptosis. It also discusses potential treatment strategies, such as antioxidants and renin-angiotensin system inhibitors, and highlights the association between sorafenib-induced hypertension and treatment efficacy in cancer patients. Furthermore, emerging research suggests a link between sorafenib-induced glycolysis, drug resistance, and cardiovascular toxicity, necessitating further investigation. Overall, understanding these mechanisms is crucial for optimizing sorafenib therapy and minimizing cardiovascular risks in cancer patients.
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What OpenQuestion 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 OpenQuestion graph.