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Chronic doxorubicin cardiotoxicity is mediated by oxidative DNA damage-ATM-p53-apoptosis pathway and attenuated by pitavastatin through the inhibition of Rac1 activity

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TLDR
Doxorubicin-induced cardiotoxicity is mediated by oxidative DNA damage-ATM-p53-apoptosis pathway, and is attenuated by pitavastatin through its antioxidant effect involving Rac1 inhibition.
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This article is published in Journal of Molecular and Cellular Cardiology.The article was published on 2009-11-01. It has received 164 citations till now. The article focuses on the topics: Cardiotoxicity & Oxidative stress.

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Nuclear-targeted drug delivery of TAT peptide-conjugated monodisperse mesoporous silica nanoparticles.

TL;DR: TAT peptide has been employed to conjugate onto mesoporous silica nanoparticles (MSNs-TAT) with high payload for nuclear-targeted drug delivery for the first time, and may provide an effective strategy for the design and development of cell-nuclear-targeting drug delivery.
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Core/Shell Structured Hollow Mesoporous Nanocapsules: A Potential Platform for Simultaneous Cell Imaging and Anticancer Drug Delivery

TL;DR: The capability of Fe(3)O(4)@mSiO(2) nanocapsules as contrast agents of MRI was demonstrated both in vitro and in vivo, indicating the simultaneous imaging and therapeutic multifunctionalities of the composite nanocapules.
Journal ArticleDOI

Drug-induced oxidative stress and toxicity.

TL;DR: The nature of ROS-induced damage on key cellular targets of oxidative stress is examined and evidence implicating ROS in clinically relevant, drug-related side effects including doxorubicin-induced cardiac damage, azidothymidine-induced myopathy, and cisplatin-induced ototoxicity is reviewed.
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Doxorubicin-induced cardiotoxicity: from bioenergetic failure and cell death to cardiomyopathy.

TL;DR: What is known about some of the potential mechanisms of DOX‐induced cardiotoxicity including mitochondrial oxidative damage and loss of cardiomyocytes are discussed and pharmaceutical and nonpharmaceutical approaches that may decrease DOX cardiac alterations in animal models and humans are presented.
References
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Journal ArticleDOI

Anthracyclines: Molecular Advances and Pharmacologic Developments in Antitumor Activity and Cardiotoxicity

TL;DR: An overview of issues confirms that anthracyclines remain “evergreen” drugs with broad clinical indications but have still an improvable therapeutic index.
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DNA damage-induced cell death by apoptosis.

TL;DR: DNA damage-triggered signaling and execution of apoptosis is cell-type- and genotoxin-specific depending on the p53 (p63 and p73) status, death-receptor responsiveness, MAP-kinase activation and, most importantly, DNA repair capacity.
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Stroke protection by 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase inhibitors mediated by endothelial nitric oxide synthase

TL;DR: In this paper, the authors showed that 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase inhibitors are not associated with changes in serum cholesterol levels, but are reversed by cotreatment with l-mevalonate and by the downstream isoprenoid, geranylgeranyl pyrophosphate.

Stroke protection by 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase inhibitors mediated by endothelial nitric oxide synthase (cerebral blood f lowycerebral ischemia)

TL;DR: The results suggest that HMG-CoA reductase inhibitors provide a prophylactic treatment strategy for increasing blood flow and reducing brain injury during cerebral ischemia.
Journal ArticleDOI

p53-induced inhibition of Hif-1 causes cardiac dysfunction during pressure overload

TL;DR: It is shown that cardiac angiogenesis is crucially involved in the adaptive mechanism of cardiachypertrophy and that p53 accumulation is essential for the transition from cardiac hypertrophy to heart failure and that the anti-angiogenic property of p53 may have a crucial function in the transition.
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