ArticleJournal of the American Heart Association2021
Carfilzomib Treatment Causes Molecular and Functional Alterations of Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes.
Article in Journal of the American Heart Association, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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
29 citing papers in PubMed, 34 citations in OpenAlex.
- Risk factors for carfilzomib-related cardiovascular adverse events in Chinese patients with multiple myeloma: A real-world retrospective cohort study.The Journal of international medical research · 2026Observational
- Cardiotoxicity of Targeted Therapies in Hematologic Malignancies: From Molecular Mechanisms to Clinical Management.Current treatment options in oncology · 2026Review
- Cardiotoxicity induced by multiple myeloma therapies: mechanistic convergence across proteasome inhibitors, CAR-T, and bispecific antibodies.Blood cancer journal · 2026Review
- Proteasome Targeting with Carfilzomib Induces Reactive Oxygen Species-Mediated Apoptosis in Hepatoblastoma.Cells · 2026Article
- Atorvastatin Protects Against Deleterious Carfilzomib-Induced Transcriptional Changes in Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes.International journal of molecular sciences · 2026Article
- Per- and Polyfluoroalkyl Substances Induce Cardiotoxicity and Alter Protein Profiles of Extracellular Matrix, Metabolism, and Mitochondrial Function in Human Cardiomyocytes.Chemical research in toxicology · 2026Article
- Carfilzomib-induced sinus bradycardia: A case report and literature review.SAGE open medical case reports · 2026Article
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- Spaceflight alters protein levels and gene expression associated with stress response and metabolic characteristics in human cardiac spheroids.Biomaterials · 2025Article
- Highly specific Immunoproteasome inhibitor M3258 induces proteotoxic stress and apoptosis in KMT2A::AFF1 driven acute lymphoblastic leukemia.Scientific reports · 2025Article
- Methodological Aspects of μLC-MS/MS for Wide-Scale Proteomic Analysis of Anthracycline-Induced Cardiomyopathy.ACS omega · 2025Article
- The Role of the Ubiquitin System in Eye Diseases.Life (Basel, Switzerland) · 2025Review
- Ethanol exposure during differentiation of human induced pluripotent stem cells reduces cardiomyocyte generation and alters metabolism.Life sciences · 2025Article
- Identifying common pathways for doxorubicin and carfilzomib-induced cardiotoxicities: transcriptomic and epigenetic profiling.Scientific reports · 2025Article
- Carfilzomib in multiple myeloma: unraveling cardiac toxicities - from mechanisms to diagnosis and management.Frontiers in pharmacology · 2025Review
- Atrial fibrillation in cancer, anticancer therapies, and underlying mechanisms.Journal of molecular and cellular cardiology · 2024Review
- Is There a Mitochondrial Protection via Remote Ischemic Conditioning in Settings of Anticancer Therapy Cardiotoxicity?Current heart failure reports · 2024Review
- Simultaneous proteome localization and turnover analysis reveals spatiotemporal features of protein homeostasis disruptions.Nature communications · 2024Article
- Cardiovascular Toxicity of Antineoplastic Treatments in Hematological Diseases: Focus on Molecular Mechanisms to Improve Therapeutic Management.Journal of clinical medicine · 2024Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Background Anticancer therapies have significantly improved patient outcomes; however, cardiac side effects from cancer therapies remain a significant challenge. Cardiotoxicity following treatment with proteasome inhibitors such as carfilzomib is known in clinical settings, but the underlying mechanisms have not been fully elucidated. Methods and Results Using human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) as a cell model for drug-induced cytotoxicity in combination with traction force microscopy, functional assessments, high-throughput imaging, and comprehensive omic analyses, we examined the molecular mechanisms involved in structural and functional alterations induced by carfilzomib in hiPSC-CMs. Following the treatment of hiPSC-CMs with carfilzomib at 0.01 to 10 µmol/L, we observed a concentration-dependent increase in carfilzomib-induced toxicity and corresponding morphological, structural, and functional changes. Carfilzomib treatment reduced mitochondrial membrane potential, ATP production, and mitochondrial oxidative respiration and increased mitochondrial oxidative stress. In addition, carfilzomib treatment affected contractility of hiPSC-CMs in 3-dimensional microtissues. At a single cell level, carfilzomib treatment impaired 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.