ArticleInternational journal of molecular sciences2022
Venetoclax Induces Cardiotoxicity through Modulation of Oxidative-Stress-Mediated Cardiac Inflammation and Apoptosis via NF-κB and BCL-2 Pathway.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- Cardiovascular Challenges in Chronic Lymphocytic Leukemia (CLL) Patients Undergoing Bruton Tyrosine Kinase (BTK) Inhibitor Therapy.European journal of haematology · 2026Pooled it
- Inflammation as a central driver in AML pathogenesis and therapy resistance.Science China. Life sciences · 2026Review
- Comment on AlAsmari et al. Venetoclax Induces Cardiotoxicity through Modulation of Oxidative-Stress-Mediated Cardiac Inflammation and Apoptosis via NF-κB and BCL-2 Pathway.International journal of molecular sciences · 2026Article
- Reply to Trela, B.A.; Guffroy, M.R. Comment on "AlAsmari et al. Venetoclax Induces Cardiotoxicity Through Modulation of Oxidative-Stress-Mediated Cardiac Inflammation and Apoptosis via NF-κB and BCL-2 Pathway.International journal of molecular sciences · 2026Article
- Impact of CaInternational journal of molecular sciences · 2026Review
- Cardiovascular Events in Patients With Acute Myeloid Leukemia Treated With Venetoclax: A Multicenter Cohort Study.JACC. Advances · 2026Article
- Cardiotoxicity induced by multiple myeloma therapies: mechanistic convergence across proteasome inhibitors, CAR-T, and bispecific antibodies.Blood cancer journal · 2026Review
- Cardiovascular Adverse Events During Venetoclax-Based Treatment in Acute Myeloid Leukemia.Journal of the American Heart Association · 2026Article
- Integrative network toxicology, molecular dynamics and transcriptional analysis elucidate DEHP-induced cardiovascular dysfunction.Toxicology research · 2025Article
- Safe administration of venetoclax-obinutuzumab in a chronic lymphocytic leukemia patient with Brugada syndrome.Annals of hematology · 2025Article
- Treatment outcomes and safety of reduced‑dose venetoclax plus antifungal agents to treat acute myeloid leukemia: A single hospital experience in Taiwan.Oncology letters · 2025Article
- Ameliorative Effect of N-Acetylcysteine Against 5-Fluorouracil-Induced Cardiotoxicity via Targeting TLR4/NF-κB and Nrf2/HO-1 Pathways.Medicina (Kaunas, Lithuania) · 2025Article
- Acute and Chronic Cardiovascular Adverse Events in Patients with Acute Myeloid Leukemia: A Systematic Review.Cancers · 2025Review
- Chronic Lymphocytic Leukemia Care and Beyond: Navigating the Needs of Long-Term Survivors.Cancers · 2025Review
- Baicalin reduces sunitinib-induced cardiotoxicity in renal carcinoma PDX model by inhibiting myocardial injury, apoptosis and fibrosis.Frontiers in pharmacology · 2025Article
- Safety of venetoclax in real-world experience: data from the French national database of pharmacovigilance through all indications in hematological malignancies over 5 years.Therapeutic advances in hematology · 2025Article
- Cardiotoxicity of venetoclax in patients with acute myeloid leukemia: comparison with anthracyclines.Cardio-oncology (London, England) · 2024Article
- Fatal heart tamponade during induction treatment with azacitidine and venetoclax.Annals of hematology · 2024Article
- Cardiovascular Toxicity of Antineoplastic Treatments in Hematological Diseases: Focus on Molecular Mechanisms to Improve Therapeutic Management.Journal of clinical medicine · 2024Review
- Society for Cardiovascular Magnetic Resonance 2024 Cases of SCMR case series.Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic ResonanceReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Cardiovascular damage induced by anticancer therapy has become the main health problem after tumor elimination. Venetoclax (VTX) is a promising novel agent that has been proven to have a high efficacy in multiple hematological diseases, especially acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL). Considering its mechanism of action, the possibility that VTX may cause cardiotoxicity cannot be ruled out. Therefore, this study was designed to investigate the toxic effect of VTX on the heart. Male Sprague-Dawley rats were randomly divided into three groups: control, low-dose VTX (50 mg/kg via oral gavage), and high-dose VTX (100 mg/kg via oral gavage). After 21 days, blood and tissue samples were collected for histopathological, biochemical, gene, and protein analyses. We demonstrated that VTX treatment resulted in cardiac damages as evidenced by major changes in histopathology and markedly elevated cardiac enzymes and hypertrophic genes markers. Moreover, we observed a drastic increase in oxidative stress, as well as inflammatory and apoptotic markers, with a remarkable decline in the levels of
Indexed as
Identifiers
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.