ArticleMolecular and cellular biochemistry2021
RIP1/RIP3/MLKL-mediated necroptosis contributes to vinblastine-induced myocardial damage.
Article in Molecular and cellular biochemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 37 citations in OpenAlex.
- Suppression of Calpain Attenuates Coxsackievirus B3-Induced Myocarditis by Regulating RIPK1/RIPK3/MLKL Pathway.Journal of cardiovascular translational research · 2026Article
- Naoluotong granules inhibit necroptosis of neural cells and improve cerebral ischemia-reperfusion injury by regulating the RIP1/NIK/IKKα/NF-κB pathway.Histology and histopathology · 2026Article
- MLKL Deficiency Stabilizes RIP3 and Aggravates Myocardial Injury by Promoting Apoptosis and Pyroptosis.Current issues in molecular biology · 2026Article
- Integration of cAMP and TRPV4 Signaling to Optimize Collagen Remodeling for Management of Fibrosis.Cells · 2025Review
- ROS-Mediated Necroptosis Promotes Coxsackievirus B3 Replication and Myocardial Injury.Microorganisms · 2025Article
- IBCar: Potent Orally Bioavailable MethylCancers · 2025Article
- Necroptosis in myocardial ischaemia-reperfusion injury: current update on mechanisms, therapeutic targets, and translational potential.Apoptosis : an international journal on programmed cell death · 2025Review
- Ethyl Pyruvate as a Potential Therapeutic Agent for Endometriosis: A Perspective.Reproductive sciences (Thousand Oaks, Calif.) · 2025Review
- Article
- Mechanism of Artemisia annua L. in the treatment of acute myocardial infarction: network pharmacology, molecular docking and in vivo validation.Molecular diversity · 2024Article
- Advanced Application of Polymer Nanocarriers in Delivery of Active Ingredients from Traditional Chinese Medicines.Molecules (Basel, Switzerland) · 2024Review
- Human adipose-derived stem cells genetically programmed to induce necroptosis for cancer immunotherapy.Cancer gene therapy · 2024Article
- Cardiac toxicity of brentuximab vedotin: a real-word disproportionality analysis of the FDA Adverse Event Reporting System (FAERS) database.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Silibinin, Synergistically Enhances Vinblastine-Mediated Apoptosis in Triple Negative Breast Cancer Cell Line: Involvement of Bcl2/Bax and Caspase-3 Pathway.International journal of hematology-oncology and stem cell research · 2024Article
- Cell death in atherosclerosis.Cell cycle (Georgetown, Tex.) · 2024Review
- Advanced application of nanotechnology in active constituents of Traditional Chinese Medicines.Journal of nanobiotechnology · 2023Review
- Circ_0000419 acts as a tumor suppressor in gastric cancer development via regulating miR-300/RGMB axis.International journal of clinical oncology · 2023Article
- Role of RIPK3‑CaMKII‑mPTP signaling pathway‑mediated necroptosis in cardiovascular diseases (Review).International journal of molecular medicine · 2023Review
- Identification and validation of a necroptosis-related gene prognostic signature for colon adenocarcinoma.Translational cancer research · 2023Article
- Skp2-mediated MLKL degradation confers cisplatin-resistant in non-small cell lung cancer cells.Communications biology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Vinblastine (VBL) has been considered as a first-line anti-tumor drug for many years. However, vinblastine-caused myocardial damage has been continually reported. The underlying molecular mechanism of the myocardial damage remains unknown. Here, we show that vinblastine induces myocardial damage and necroptosis is involved in the vinblastine-induced myocardial damage both in vitro and in vivo. The results of WST-8 and flow cytometry analysis show that vinblastine causes damage to H9c2 cells, and the results of animal experiments show that vinblastine causes myocardial cell damage. The necrosome components, receptor-interacting protein 1 (RIP1) receptor-interacting protein 3 (RIP3), are significantly increased in vinblastine-treated H9c2 cells, primary neonatal rat ventricular myocytes and rat heart tissues. And the downstream substrate of RIP3, mixed lineage kinase domain like protein (MLKL) was also increased. Pre-treatment with necroptosis inhibitors partially inhibits the necrosome components and MLKL levels and alleviates vinblastine-induced myocardial injury both in vitro and in vivo. This study indicates that necroptosis participated in vinblastine-evoked myocardial cell death partially, which would be a potential target for relieving the chemotherapy-related myocardial damage.
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.