Differences in doxorubicin-induced apoptotic signaling in adult and immature cardiomyocytes.
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TL;DR: In this article, the authors investigated the molecular basis for the differences in DOX-induced toxicity in adult rat cardiomyocytes (ARCM), neonatal rat Cardiomyocyte (NRCM), and rat embryonic H9c2 cardiomaoblasts.
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About: This article is published in Free Radical Biology and Medicine. The article was published on 15 Dec 2008. and is currently open access. The article focuses on the topics: XIAP & APAF1.
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Citations
Cardiomyocyte death in doxorubicin-induced cardiotoxicity
TL;DR: Current understanding of the molecular mechanisms underlying DOX-induced cardiomyocyte death, including the major primary mechanism of excess production of reactive oxygen species (ROS) and other recently discovered ROS-independent mechanisms are focused on.
Prodeath Signaling of G Protein-Coupled Receptor Kinase 2 in Cardiac Myocytes After Ischemic Stress Occurs via Extracellular Signal-Regulated Kinase-Dependent Heat Shock Protein 90-mediated Mitochondrial Targeting
Mai Chen,Priscila Y. Sato,J. Kurt Chuprun,Raymond J. Peroutka,Nicholas J. Otis,Jessica Ibetti,Shi Pan,Shey-Shing Sheu,Erhe Gao,Walter J. Koch +9 more
TL;DR: G protein–coupled receptor kinase 2 is identified as a prodeath kinase in the heart, acting in a novel manner through mitochondrial localization via extracellular signal–regulated kinase regulation.
140
Tannic acid ameliorates doxorubicin-induced cardiotoxicity and potentiates its anti-cancer activity: Potential role of tannins in cancer chemotherapy
TL;DR: This is the first report which shows that tannic acid ameliorates doxorubicin-induced cardiotoxicity and potentiates its anti-cancer activity both in vitro (H9c2 and MDA-MB-231 cells) as well as in in vivo model of DMBA-induced mammary tumor animals.
118
Doxorubicin impairs cardiomyocyte viability by suppressing transcription factor EB expression and disrupting autophagy
Jordan J. Bartlett,Purvi C. Trivedi,Pollen K.F. Yeung,Petra C. Kienesberger,Thomas Pulinilkunnil +4 more
TL;DR: It is found that DOX repressed cellular TFEB expression, which was associated with impaired cathepsin proteolytic activity across in vivo, ex vivo, and in vitro models of DOX cardiotoxicity, revealing a novel mechanism wherein DOX primes cardiomyocytes for cell death by depleting cellular T FEB.
109
Effects of doxorubicin cancer therapy on autophagy and the ubiquitin-proteasome system in long-term cultured adult rat cardiomyocytes.
Polychronis Dimitrakis,Maria-Iris Romay-Ogando,Francesco Timolati,Thomas M. Suter,Christian Zuppinger +4 more
TL;DR: Doxo causes a downregulation of the protein degradation machinery of cardiomyocytes with a resulting accumulation of poly-ubiquitinated proteins and autophagosomes, which might contribute to the late cardiotoxicity of anthracyclines by accelerated aging of the postmitotic adult card iomyocytes and to the susceptibility of the aging heart to anthRacycline cancer therapy.
References
Non-Endocrine Late Complications of Bone Marrow Transplantation in Childhood: Part I
Ad Leiper
TL;DR: This study reviews non-endocrine late complications of bone marrow transplantation (BMT) in childhood, including ocular, audiological, dental, salivary, and skeletal toxicity, second malignant neoplasms, overall morbidity, late mortality, and quality of life. Common complications include cataracts, keratoconjunctivitis sicca, hearing loss, dental abnormalities, salivary dysfunction, avascular necrosis of bone, and multiple osteochondromas.
Human skeletal muscle cytosols are refractory to cytochrome c-dependent activation of type-II caspases and lack APAF-1.
David H. Burgess,Michael Svensson,Tiziana Dandrea,Karina Grönlund,Folke Hammarquist,Sten Orrenius,Ian A. Cotgreave +6 more
TL;DR: It is demonstrated that cytosols from skeletal muscle biopsies from healthy human volunteers lack the ability to activate type-II caspases by a cytochrome c-mediated pathway despite the confirmed presence of both procaspase-3 and -9, and that human skeletal muscle cells can escape a major pro-apoptotic regulatory mechanism.
Daunorubicin-Induced Apoptosis in Rat Cardiac Myocytes Is Inhibited by Dexrazoxane
TL;DR: The recognition that anthracycline-induced cardiac myocyte apoptosis occurs at concentrations well below those that result in myocyte necrosis, may aid in the design of new therapeutic strategies to limit the toxicity of these drugs.
A clinicopathologic analysis of adriamycin cardiotoxicity
TL;DR: It is suggested that the total dose of adriamycin should be limited to less than 550 mg/m2 to permit safer use of this efficacious cancer chemotherapeutic agent.
•Journal Article
p53 mediates DNA damaging drug-induced apoptosis through a caspase-9-dependent pathway in SH-SY5Y neuroblastoma cells
TL;DR: A molecular pathway for mediating DNA damaging drug-induced apoptosis in the human neuroblastoma SH-SY5Y cells is defined and inactivation of essential components of this apoptotic pathway may confer drug resistance on neuroblastomas cells.