Literatura científica selecionada sobre o tema "Cardiotoxicité Induite par la DOX"
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Artigos de revistas sobre o assunto "Cardiotoxicité Induite par la DOX"
Mechri, A., A. Amrani, W. Benabderrahmane, O. Benaissa, N. Boubekri, D. Zama, F. Benayache e S. Benayache. "Les polyphénols de l’extrait n-butanol de Crataegus oxyacantha : évaluation de leur pouvoir antioxydant et protecteur vis-à-vis de la toxicité de la doxorubicine". Phytothérapie 16, S1 (28 de setembro de 2018): S22—S31. http://dx.doi.org/10.3166/phyto-2018-0009.
Texto completo da fonteGouttebel, Marie-Claude, Guo Hua Zhang, Bernard Saingra e Henri Joyeux. "Rôle protecteur d'un apport oral de sélénium et de vitamine E vis-à-vis de la cardiotoxicité induite par les anthracyclines chez le rat". Nutrition Clinique et Métabolisme 10, n.º 2 (janeiro de 1996): 69–76. http://dx.doi.org/10.1016/s0985-0562(96)80030-6.
Texto completo da fonteWalker, V., O. Lairez, O. Fondard, G. Jimenez, D. Broggio, D. Laurier, J. Ferrières e S. Jacob. "Utilisation de l’imagerie 2D-strain du myocarde pour la détection précoce de la cardiotoxicité induite par la radiothérapie chez les patientes atteintes d’un cancer du sein (étude BACCARAT)". Revue d'Épidémiologie et de Santé Publique 67 (maio de 2019): S155—S156. http://dx.doi.org/10.1016/j.respe.2019.03.032.
Texto completo da fonteTeses / dissertações sobre o assunto "Cardiotoxicité Induite par la DOX"
Mammadova, Aynura. "The role of MEIS inhibitors in cardiac regeneration and protection". Electronic Thesis or Diss., Strasbourg, 2024. http://www.theses.fr/2024STRAJ006.
Texto completo da fonteThe 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
Mazevet, Marianne. "Etude de la cardiotoxicité induite par les traitements anticancéreux : Rôle d’Epac dans la cardiotoxicité induite par la Doxorubicine". Thesis, Université Paris-Saclay (ComUE), 2015. http://www.theses.fr/2015SACLS190/document.
Texto completo da fonteThe mechanisms underlying doxorubicin (Dox)-induced cardiotoxicity involve reactive oxygen species generation, DNA intercalation and topoisomerase II (TopII) inhibition which trigger DNA damage, oxidative stress, alteration of calcium homeostasis and lead to cardiomyocyte death. Now, evidences have emerged that Dox may promote cardiotoxicity by alternative mechanisms or by signaling pathways modulation including β-adrenergic signaling unrelated directly to cell death. This study provides in vitro and in vivo evidence of the guanine exchange factor directly activated by Epac role, a guanine exchange factor directly activated by cyclic AMP produced after β-AR stimulation, in cardiotoxicity induced by doxorubicin. Indeed, Dox leads to the development of a dilated cardiomyopathy (DCM) 15 weeks post treatment in mice associated with calcium homeostasis abnormalities. These alterations were associated with time- and dose-dependent alterations of Epac signaling. The same alterations of Epac signaling were observed in vitro after 24h of dox treatment. Furthermore, we first showed that the specific pharmacologic or genetic inhibition of Epac1 but not Epac2 prevents the deleterious effects of Dox in vitro. These cardioprotection were confirmed in vivo in transgenic Knock-out Epac1 mice. Epac 1 inhibition did not interfere with the attempted Dox antitumor efficiency on tumor cell lines. Altogether, these findings identify the cAMP-binding protein, Epac, as a potential therapeutic target of dox-induced cardiotoxicity
Ribeiro, Maxance. "EPAC1 : une nouvelle cible thérapeutique pour limiter la cardiotoxicité induite par les Anthracyclines". Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLS509/document.
Texto completo da fonteDoxorubicin (Dox) is an Anthracycline commonly used to treat many types of cancer; unfortunately this chemotherapeutic agent often induces side effects such as cardiotoxicity leading to cardiomyocyte death and dilated cardiomyopathy (DCM). This cardiotoxicity has been related to reactive oxygen species generation, DNA intercalation, topoisomerase II inhibition and bioenergetics alterations resulting in DNA damages and ultimately in cardiomyocyte death. Nevertheless, complete molecular mechanisms are not yet identified. Therefore, there is a need for new treatment options and strategies aiming at reducing Dox side effects in the heart. Among these mechanisms, EPAC1 (Exchange Protein directly Activated by cAMP) signaling could be worth investigating as EPAC1 indirectly activates small G proteins (Rac1 and Rho A), which are known to be involved in Dox-induced cardiotoxicity. Therefore, we have investigated the effect of Dox on EPAC1 signaling in both in vivo mice model (C57BL/6 vs EPAC1 KO mice, iv injections, 12mg/kg) and in vitro model (primary culture of neonatal rat cardiomyocytes (NRVM), Dox 1μM). In vivo, Dox-treated mice developed a DCM associated with Ca2+ homeostasis dysfunction. In vitro, Dox induced DNA damages and cell death associated with huge mitochondrial disorders, characterized by a decrease in mitochondrial biogenesis and respiratory chain activity. This cell death is associated with apoptotic features including mitochondrial membrane permeabilization, caspase activation, cell size reduction and relative plasma membrane integrity. We also observed that Dox led to a modification of the protein level and the activity of EPAC1 in the same manner to the cAMP level. By contrast, the inhibition of EPAC1, prevented DNA/TopIIβ complexes, decreased Dox-induced DNA damages, loss of mitochondrial membrane potential, apoptosis and finally cardiomyocyte death. Mitochondrial biogenesis and respiratory chain activity operated normally when EPAC1 was inhibited. These results were confirmed in vivo since Dox-induced cardiotoxicity was prevented in EPAC1 KO mice as evidenced by unaltered cardiac function (no DCM) at 15 weeks post-treatment. Interestingly, the protection conferred by EPAC1 inhibition was not transferred in human cancer cell lines treated by Dox. Inhibition of EPAC1 could thus be a valuable therapeutic strategy to limit Dox-induced cardiomyopathy during cancer chemotherapy
Merlet, Nolwenn. "Altération du système bêta-adrénertique cardiaque au cours de la cardiotoxicité induite par la doxorubicine". Nantes, 2011. http://www.theses.fr/2011NANT2058.
Texto completo da fonteAnthracyclines, like doxorubicin (Dox), are very efficient chemotherapeutic agents but there use is limited by the possible development of severe cardiotoxicity leading to progressive and irreversible heart failure (HF). A recent clinical trial reported that early administration of angiotensin converting enzyme inhibitor associated with β-blocker can improve cardiac function of those patients with HF due to dox (Dox-HF), meaning an important role of β-adrenergic (β-AR) system in this pathology, The aim of this PhD work was to develop a rat model of early chronic Dox-cardiotoxicity and then to assess cardiac β-AR system in this model. Thus, we observed that β1-AR expression was decreased but its function was preserved, due to an increased adenylyl cyclase activity β2-AR expression was increased and was correlated with an increased function. Finally, neither β3-AR expression nor function were altered in our model. Thus, Dox-HF is characterized by an important cardiac β-AR system remodeling, as described in other forms of HF. At end stage of human HF, a β1-AR down-expression and a β3-AR over-expression was described. However, the precise role of each cardiac βAR in HF development is weakly known. In a healthy rat model, we plan to modulate cardiac β-AR expressions (over-expression by adenoviral vector or down-expression by siRNA) and to assess the consequences on hemodynamic parameters and cardiac β-AR remodeling. In this context, the second aim of this PhD work was to develop an intracardiac injection method in rat, using an adenoviral vector
Gascon, Suzanne. "Développement d’un modèle de suivi en imagerie TEP de la cardiotoxicité induite par chimiothérapie chez la souris". Mémoire, Université de Sherbrooke, 2015. http://hdl.handle.net/11143/6613.
Texto completo da fonteWalker, Valentin. "Étude du risque de cardiotoxicité radio-induite précoce chez des patientes traitées par radiothérapie pour un cancer du sein à partir de la cohorte prospective BACCARAT Early Detection of Cardiovascular Changes After Radiotherapy for Breast Cancer: Protocol for a European Multicenter Prospective Cohort (MEDIRAD EARLY HEART Study) Early Detection of Subclinical Left Ventricular Dysfunction After Breast Cancer Radiation Therapy Using Speckle-tracking Echocardiography: Association between Cardiac Exposure and Longitudinal Strain Changes (BACCARAT Study)". Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASR003.
Texto completo da fonteRadiation therapy (RT), an adjuvant treatment for breast cancer, is associated with an increased risk of cardiovascular disease several years after RT. Identifying early signs of cardiotoxicity and their relationship to the dose of ionizing radiation absorbed by the heart could help predict the occurrence of cardiovascular disease and improve prevention in patients at risk.This thesis is based on the BACCARAT cohort that included a hundred of patients treated with breast RT without chemotherapy and followed during 24 months post-RT. An individual reconstitution of the doses absorbed by the heart, the left ventricle (LV) and the coronary arteries was performed.Early signs of cardiotoxicity were defined by subclinical cardiac dysfunctions evaluated by echocardiography and by changes in the concentrations of a panel of circulating biomarkers potentially involved in cardiotoxicity.With an intermediate follow-up of 6 months, the analysis of data showed a dose-response relationship between subclinical left ventricular dysfunction characterized by a >10% decrease in the myocardial contractility index (longitudinal strain) and the average dose absorbed by the LV. The alteration of fibrinogen levels at the end of RT, combined with the LV dose, improved risk prediction (based on longitudinal strain)