ArticleJournal of translational medicine2023
WGX50 mitigates doxorubicin-induced cardiotoxicity through inhibition of mitochondrial ROS and ferroptosis.
Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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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.
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Who cites it
62 citing papers in PubMed, 112 citations in OpenAlex.
- Breaking the cycle of fibrosis: Ferroptosis as a therapeutic target (Review).International journal of molecular medicine · 2026Review
- Dexpanthenol Attenuates Doxorubicin-Induced Cardiotoxicity by Modulating Oxidative Stress, Inflammation, and Apoptosis.Cardiovascular toxicology · 2026Article
- Multidimensional perspectives on cancer therapy-induced cardiotoxicity: Characteristics, mechanisms, biomarkers, psychological stress effects, and treatment progress.Cancer pathogenesis and therapy · 2026Review
- Calycosin Safeguards Mitochondrial Genomic Stability and Iron Homeostasis via the NRF2/NRF1-TFAM Axis to Mitigate Doxorubicin-Induced Cardiotoxicity.Antioxidants (Basel, Switzerland) · 2026Article
- Quercetin Activates NRF2/SLC7A11/GPX4 Signaling to Restore Mitochondrial Function Inhibit Ferroptosis Thereby Alleviating Doxorubicin-Induced Cardiotoxicity.Biomolecules · 2026Article
- Morroniside Attenuates Doxorubicin-Induced Cardiotoxicity by Activating the PI3K/AKT/Nrf2/HO-1 Pathway to Inhibit Ferroptosis and Oxidative Stress.Journal of biochemical and molecular toxicology · 2026Article
- Identification of TGF-β1 as a key regulator in DOX-induced cardiotoxicity.Journal of cardiothoracic surgery · 2026Article
- Carfilzomib Induces Cardiotoxicity by Blocking Autophagic Flux Through the cGAS-STING Signaling Pathway.Biomolecules · 2026Article
- Metabolic regulation of ferroptosis in cancer: mechanisms, pharmacological inducers, and translational challenges.Apoptosis : an international journal on programmed cell death · 2026Review
- KLF9 Aggravates Doxorubicin-Induced Cardiotoxicity by Regulating the ROS/p53 Signalling Pathway.Cardiovascular toxicology · 2026Article
- Dapagliflozin Protects Cardiomyocytes against Doxorubicin-Induced Toxicity by Modulating Sirtuin 1/Sirtuin 3 and Ferroptosis Pathway.ACS pharmacology & translational science · 2026Article
- Cardiac reprogramming via transient overexpression of P-glycoprotein alleviates doxorubicin-induced cardiotoxicity in mice and pigs.Nature communications · 2026Article
- Contrastive representation learning and capsule networks enable accurate identification of ferroptosis-related proteins.Journal of cheminformatics · 2026Article
- Persistently increased CaMKIIδ autophosphorylation mediates pathologic SR Ca loss in a murine model of Doxorubicin-induced cardiomyopathy.Journal of molecular and cellular cardiology plus · 2026Article
- NFS1 Regulates IDH2 to Attenuate Abdominal Aortic Aneurysms via Interacting With SP2.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeted Nanodelivery of WGX50 and Curcumin via Gold Nanoparticles for Alzheimer's Therapy.Journal of cellular and molecular medicine · 2026Article
- Doxorubicin-Induced Cardiac Remodeling: Mechanisms and Mitigation Strategies.Cardiovascular drugs and therapy · 2026Review
- Review
- Hydrogen treatment attenuates ferroptosis and alleviates spinal cord ischemia-reperfusion injury by activating the Nrf2/HO-1 signaling pathway.Molecular biology reports · 2026Article
- Hyperoside Inhibits Doxorubicin-Induced Ferroptosis in Cardiomyocytes via the Nrf2/GPX4 Pathway.Journal of cardiovascular translational research · 2026Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
29 authors at 6 institutions in 2 countries.
Funding
Abstract
backgroundDoxorubicin (DOX)-induced cardiotoxicity (DIC) is a major impediment to its clinical application. It is indispensable to explore alternative treatment molecules or drugs for mitigating DIC. WGX50, an organic extract derived from Zanthoxylum bungeanum Maxim, has anti-inflammatory and antioxidant biological activity, however, its function and mechanism in DIC remain unclear.
methodsWe established DOX-induced cardiotoxicity models both in vitro and in vivo. Echocardiography and histological analyses were used to determine the severity of cardiac injury in mice. The myocardial damage markers cTnT, CK-MB, ANP, BNP, and ferroptosis associated indicators Fe
resultsOur findings demonstrate that WGX50 protects DOX-induced cardiotoxicity via restraining mitochondrial ROS and ferroptosis. In vivo, WGX50 effectively relieves doxorubicin-induced cardiac dysfunction, cardiac injury, fibrosis, mitochondrial damage, and redox imbalance. In vitro, WGX50 preserves mitochondrial function by reducing the level of mitochondrial membrane potential and increasing mitochondrial ATP production. Furthermore, WGX50 reduces iron accumulation and mitochondrial ROS, increases GPX4 expression, and regulates lipid metabolism to inhibit DOX-induced ferroptosis.
conclusionTaken together, WGX50 protects DOX-induced cardiotoxicity via mitochondrial ROS and the ferroptosis pathway, which provides novel insights for WGX50 as a promising drug candidate for cardioprotection.
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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.