Gotowa bibliografia na temat „Dox-Induced Cardiotoxicity”
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Artykuły w czasopismach na temat "Dox-Induced Cardiotoxicity"
Sumneang, Natticha, Pongpan Tanajak i Thura Tun Oo. "Toll-like Receptor 4 Inflammatory Perspective on Doxorubicin-Induced Cardiotoxicity". Molecules 28, nr 11 (24.05.2023): 4294. http://dx.doi.org/10.3390/molecules28114294.
Pełny tekst źródłaAmmar, El-Sayed M., Shehta A. Said, Ghada M. Suddek i Sally L. El-Damarawy. "Amelioration of doxorubicin-induced cardiotoxicity by deferiprone in rats". Canadian Journal of Physiology and Pharmacology 89, nr 4 (kwiecień 2011): 269–76. http://dx.doi.org/10.1139/y11-020.
Pełny tekst źródłaHamaamin, Karmand Salih, i Tavga Ahmed Aziz. "Doxorubicin-Induced Cardiotoxicity: Mechanisms and Management". Al-Rafidain Journal of Medical Sciences ( ISSN: 2789-3219 ) 3 (10.12.2022): 87–97. http://dx.doi.org/10.54133/ajms.v3i.90.
Pełny tekst źródłaZheng, Dong, Yi Zhang, Ming Zheng, Ting Cao, Grace Wang, Lulu Zhang, Rui Ni i in. "Nicotinamide riboside promotes autolysosome clearance in preventing doxorubicin-induced cardiotoxicity". Clinical Science 133, nr 13 (lipiec 2019): 1505–21. http://dx.doi.org/10.1042/cs20181022.
Pełny tekst źródłaZhang, Wei, Zhixing Fan, Fengyuan Wang, Lin Yin, Jinchun Wu, Dengke Li, Siwei Song, Xi Wang, Yanhong Tang i Congxin Huang. "Tubeimoside I Ameliorates Doxorubicin-Induced Cardiotoxicity by Upregulating SIRT3". Oxidative Medicine and Cellular Longevity 2023 (14.01.2023): 1–23. http://dx.doi.org/10.1155/2023/9966355.
Pełny tekst źródłaMao, Jin Ning, Ai Jun Li, Liang Ping Zhao, Lan Gao, Wei Ting Xu, Xiao Su Hong, Wen Ping Jiang i Jian Chang Chen. "PEG-PLGA Nanoparticles Entrapping Doxorubicin Reduced Doxorubicin-Induced Cardiotoxicity in Rats". Advanced Materials Research 912-914 (kwiecień 2014): 263–68. http://dx.doi.org/10.4028/www.scientific.net/amr.912-914.263.
Pełny tekst źródłaManeechote, Chayodom, Siriporn C. Chattipakorn i Nipon Chattipakorn. "Recent Advances in Mitochondrial Fission/Fusion-Targeted Therapy in Doxorubicin-Induced Cardiotoxicity". Pharmaceutics 15, nr 4 (7.04.2023): 1182. http://dx.doi.org/10.3390/pharmaceutics15041182.
Pełny tekst źródłaKitakata, Hiroki, Jin Endo, Hidehiko Ikura, Hidenori Moriyama, Kohsuke Shirakawa, Yoshinori Katsumata i Motoaki Sano. "Therapeutic Targets for DOX-Induced Cardiomyopathy: Role of Apoptosis vs. Ferroptosis". International Journal of Molecular Sciences 23, nr 3 (26.01.2022): 1414. http://dx.doi.org/10.3390/ijms23031414.
Pełny tekst źródłada Cunha Menezes Souza, Leonardo, Meng Chen, Yuji Ikeno, Daisy Maria Fávero Salvadori i Yidong Bai. "The implications of mitochondria in doxorubicin treatment of cancer in the context of traditional and modern medicine". Traditional Medicine and Modern Medicine 03, nr 04 (grudzień 2020): 239–54. http://dx.doi.org/10.1142/s2575900020300076.
Pełny tekst źródłaJiang, Lai, Yanping Gong, Yida Hu, Yangyang You, Jiawu Wang, Zhetao Zhang, Zeyuan Wei i Chaoliang Tang. "Peroxiredoxin-1 Overexpression Attenuates Doxorubicin-Induced Cardiotoxicity by Inhibiting Oxidative Stress and Cardiomyocyte Apoptosis". Oxidative Medicine and Cellular Longevity 2020 (29.07.2020): 1–11. http://dx.doi.org/10.1155/2020/2405135.
Pełny tekst źródłaRozprawy doktorskie na temat "Dox-Induced Cardiotoxicity"
Mammadova, Aynura. "The role of MEIS inhibitors in cardiac regeneration and protection". Electronic Thesis or Diss., Strasbourg, 2024. http://www.theses.fr/2024STRAJ006.
Pełny tekst źródłaThe TALE-type homeobox gene MEIS1 has been identified as a critical factor in controlling the cell cycle arrest of cardiomyocytes, presenting itself as an attractive target for therapy. Our latest investigations have revealed the potential of MEIS1 suppression to promote the regeneration of cardiomyocytes. Further experiments with neonatal cardiomyocytes showed that two innovative small molecules, MEISi-1 and MEISi-2, enhanced the proliferation (Ph3+TnnT cells) and cytokinesis (AuroraB+TnnT cells) of these cells. Suppressing MEIS1 activity resulted in the diminished expression of its target genes and the inhibitors of cyclin-dependent kinases. Additionally, this research extended to cultivating human induced pluripotent stem cells (hiPSCs) into cardiomyocytes to examine the impact of MEIS1 suppression, which notably did not compromise their viability. Intriguingly, short-term and long-term treatment with MEISi in hiPSCs led to significant elevation in essential cardiac-specific gene expression, notably influencing cardiac mesoderm and progenitor cells, and positioning MEIS1 inhibitors as crucial modulators of cardiac gene expression. Our findings indicate that MEIS inhibitors can provide protection against the acute cardiotoxic effects of doxorubicin (DOX) in Wistar rats, as evidenced by the maintained structure of cardiac tissue and unchanged levels of fibrosis or collagen. qPCR analyses further confirmed the upregulation of cardiac progenitor genes and a balance in anti-apoptotic and ROS-related gene expression, hinting at the protective role of MEIS inhibitors against DOX-induced damage without influencing fibrosis. These results highlight the therapeutic potential of MEIS inhibitors in regenerative cardiology, suggesting their utility in enhancing cardiomyocyte renewal and offering protection against cardiotoxicity
Streszczenia konferencji na temat "Dox-Induced Cardiotoxicity"
Tao, Rong-Hua, Masato Kobayashi, Fei Wang, Yuanzheng Yang i Eugenie S. Kleinerman. "Abstract 5422: Dissecting the mechanism of exercise-mediated protection of Dox-induced cardiotoxicity". W Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-5422.
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