ArticleInternational journal of nanomedicine2017
Prevention of doxorubicin-induced cardiomyopathy using targeted MaFGF mediated by nanoparticles combined with ultrasound-targeted MB destruction.
Article in International journal of nanomedicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
- Ultrasound-targeted microbubble destruction: a prospective strategy for treating cardiovascular disease.Frontiers in cardiovascular medicine · 2025Review
- Cardiac gene delivery using ultrasound: State of the field.Molecular therapy. Methods & clinical development · 2024Review
- Puerarin inhibits NHE1 activity by interfering with the p38 pathway and attenuates mitochondrial damage induced by myocardial calcium overload in heart failure rats.Acta biochimica et biophysica Sinica · 2024Article
- Engineering Versatile Nanomedicines for Ultrasonic Tumor Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- Adriamycin induces cardiac fibrosis in mice via PRMT5-mediated cardiac fibroblast activation.Acta pharmacologica Sinica · 2023Article
- A new FGF1 variant protects against adriamycin-induced cardiotoxicity via modulating p53 activity.Redox biology · 2022Article
- Nanomaterials as Ultrasound Theragnostic Tools for Heart Disease Treatment/Diagnosis.International journal of molecular sciences · 2022Review
- Evidence for the Benefits of Melatonin in Cardiovascular Disease.Frontiers in cardiovascular medicine · 2022Review
- NMCP-2 polysaccharide purified fromFood science & nutrition · 2021Article
- Ultrasound-targeted microbubble destruction promotes myocardial angiogenesis and functional improvements in rat model of diabetic cardiomyopathy.BMC cardiovascular disorders · 2021Article
- aFGF Targeted Mediated by Novel Nanoparticles-Microbubble Complex Combined With Ultrasound-Targeted Microbubble Destruction attenuates Doxorubicin-Induced Heart Failure via Anti-Apoptosis and Promoting Cardiac Angiogenesis.Frontiers in pharmacology · 2021Article
- Article
- What is considered cardiotoxicity of anthracyclines in animal studies.Oncology reports · 2020Review
- Ultrasound-Responsive Cavitation Nuclei for Therapy and Drug Delivery.Ultrasound in medicine & biology · 2020Review
- Article
- Melatonin attenuates doxorubicin-induced cardiotoxicity through preservation of YAP expression.Journal of cellular and molecular medicine · 2020Article
- Article
- Hydrogel-Mediated DOX⋅HCl/PTX Delivery System for Breast Cancer Therapy.International journal of molecular sciences · 2019Article
- Yellow Wine Polyphenolic Compounds prevents Doxorubicin-induced cardiotoxicity through activation of the Nrf2 signalling pathway.Journal of cellular and molecular medicine · 2019Article
- Efficient treatment of Parkinson's disease using ultrasonography-guided rhFGF20 proteoliposomes.Drug delivery · 2018Article
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study seeks to observe the preventive effects of doxorubicin-induced cardiomyopathy (DOX-CM) in rats using targeted non-mitogenic acidic fibroblast growth factor (MaFGF) mediated by nanoparticles (NP) combined with ultrasound-targeted MB destruction (UTMD). DOX-CM rats were induced by intraperitoneally injected doxorubicin. Six weeks after intervention, the indices from the transthoracic echocardiography and velocity vector imaging showed that the left ventricular function in the MaFGF-loaded NP (MaFGF-NP) + UTMD group was significantly improved compared with the DOX-CM group. The increased malondialdehyde and decreased superoxide dismutase were observed in the DOX-CM group, while a significant increase in superoxide dismutase and a decrease in malondialdehyde were detected in the groups treated with MaFGF-NP + UTMD. From the Masson staining, the MaFGF-NP + UTMD group showed a significant difference from the DOX-CM group. The cardiac collagen volume fraction and the ratio of the perivascular collagen area to the luminal area number of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labelling positive cells in the MaFGF-NP + UTMD group decreased to 8.9%, 0.55-fold, compared with the DOX-CM group (26.5%, 1.7-fold). From terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labelling staining, the results showed the strongest inhibition of apoptosis progress in MaFGF-NP + UTMD group. The immunohistochemical staining of the TGF-β1 in MaFGF-NP + UTMD group reached 3.6%, which was much lower than that of the DOX-CM group (12.6%). These results confirmed that the abnormalities, including left ventricular dysfunction, myocardial fibrosis, cardiomyocytes apoptosis and oxidative stress, could be suppressed by twice weekly MaFGF treatments for 6 consecutive weeks (free MaFGF or MaFGF-NP+/UTMD), with the strongest improvements observed in the MaFGF-NP + UTMD group. Western blot analyses of the heart tissue further revealed the highest pAkt levels, highest anti-apoptosis protein (Bcl-2) levels and strongest reduction in proapoptosis protein (Bax) levels in the MaFGF-NP + UTMD group. This study confirmed the preventive effects of DOX-CM in the rats with MaFGF-NP and UTMD by retarding myocardial fibrosis, inhibiting oxidative stress, and decreasing cardiomyocyte apoptosis.
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