ArticleCardiovascular toxicology2023
Trophoblast Stem-Cell-Derived Exosomes Alleviate Cardiotoxicity of Doxorubicin via Improving Mfn2-Mediated Mitochondrial Fusion.
Article in Cardiovascular toxicology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.
- Advances in the study of exosomes in cardiovascular diseases.Journal of advanced research · 2024Pooled it
- Article
- Small Extracellular Vesicles in Cardioprotection, Cardiac Repair, and Regeneration: Cargo Mechanisms, Producer Cell Sources, and Translational Development.Biomedicines · 2026Review
- A Non-Channel Function of CFTR: Attenuating Mitochondrial Oxidative Stress and Cardiomyocyte Senescence via Stabilization by USP45.Aging cell · 2026Article
- Beyond the neuron: Exosomes as intercellular modulators of mitochondrial networks in the pathogenesis and treatment of Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Extracellular Vesicles as Biomarkers and Non-Surgical Therapeutics in Cardiovascular Diseases.Journal of clinical medicine · 2026Review
- Extracellular vesicles in heart failure: bridging pathogenic insights, diagnostic utility, and therapeutic applications.Frontiers in pharmacology · 2026Review
- Extracellular Vesicle-Based Strategies for the Prevention of Chemotherapy-Induced Cardiotoxicity.Therapeutics and clinical risk management · 2026Review
- Nanomedicine-Based Strategies for Mitigating Chemo/Radiotherapy-Induced Cardiac Inflammation and Fibrosis.Cardiovascular toxicology · 2025Review
- Potential Biomarker and Therapeutic Tools for Pathological Cardiac Hypertrophy and Heart Failure: Extracellular Vesicles.International journal of molecular sciences · 2025Review
- Targeting mitochondria to protect the heart: a matter of balance?Clinical science (London, England : 1979) · 2025Review
- Early warning of drug-induced cardiotoxicity: quantitative determination of Mfn2 biomarker via electrochemical immunosensing technology.Mikrochimica acta · 2025Article
- Trophoblast Extracellular Vesicles as Modulators of Keratinocyte Stress Response and Senescence.Life (Basel, Switzerland) · 2025Article
- Mitochondrial quality control as a therapeutic target in cardiovascular disease: Mechanistic insights and future directions.Journal of translational internal medicine · 2025Article
- Rnd3 protects against doxorubicin-induced cardiotoxicity through inhibition of PANoptosis in a Rock1/Drp1/mitochondrial fission-dependent manner.Cell death & disease · 2025Article
- Exosome-Mediated Mitochondrial Regulation: A Promising Therapeutic Tool for Alzheimer's Disease and Parkinson's Disease.International journal of nanomedicine · 2025Review
- The structure and function of mitofusin 2 and its role in cardiovascular disease through mediating mitochondria-associated endoplasmic reticulum membranes.Frontiers in cardiovascular medicine · 2025Review
- Exosomal miR-9-5p derived from iPSC-MSCs ameliorates doxorubicin-induced cardiomyopathy by inhibiting cardiomyocyte senescence.Journal of nanobiotechnology · 2024Article
- Review
- Silencing of microRNA-106b-5p prevents doxorubicin-mediated cardiotoxicity through modulation of the PR55α/YY1/sST2 signaling axis.Molecular therapy. Nucleic acids · 2023Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Doxorubicin (Dox) is an anticancer drug widely used in tumor chemotherapy, but it has the side-effect of cardiotoxicity, which is closely related to mitochondrial damage. Mitochondrial dynamics is a quality control mechanism that usually helps to maintain a healthy mitochondrial pool. Trophoblast stem cell-derived exosomes (TSC-Exos) have been shown to protect cardiomyocytes from DOX-induced cardiotoxicity. To explore whether the cardioprotective role is mediated by the regulation of mitochondrial dynamic mechanism, TSC-Exos were isolated from human trophoblast stem cells by ultracentrifugation and characterized by Western blot and transmission electron microscopy. Cellular experiments of H9c2 cardiomyocytes co-cultured with Dox and TSC-Exos were performed in vitro to determine the levels of reactive oxygen species generation and apoptosis level. An animal model of heart failure was established by intraperitoneal injection of Dox in vivo, therapy mice were received additional intracardiac injection of TSC-Exos, then, the cardiac function, cardiomyocyte apoptosis and mitochondrial fragmentation were ameliorated. Histology assays suggest that Dox caused an increased tendency of mitochondrial fission, which was manifested by a decrease in the average size of mitochondria. By receiving TSC-Exos treatment, this effect was eliminated. In summary, these results suggest that TSC-Exos alleviate DOX-induced cardiotoxicity through antiapoptotic effect and improving mitochondrial fusion with an increase in Mfn2 expression. This study is the first to provide a potential new treatment scheme for the treatment of heart failure from the perspective of the relationship between TSC-Exos and mitochondrial dynamics.
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Registered trials
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