ArticleAmerican journal of physiology. Heart and circulatory physiology2012
Downregulation of doxorubicin-induced myocardial apoptosis accompanies postnatal heart maturation.
Article in American journal of physiology. Heart and circulatory physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- ROCK1 deficiency preserves caveolar compartmentalization of signaling molecules and cell membrane integrity.FASEB bioAdvances · 2024Article
- Doxorubicin-induced cardiotoxicity and risk factors.International journal of cardiology. Heart & vasculature · 2024Article
- Endogenous and imposed determinants of apoptotic vulnerabilities in cancer.Trends in cancer · 2023Review
- Loss of Rbl2 (Retinoblastoma-Like 2) Exacerbates Myocardial Ischemia/Reperfusion Injury.Journal of the American Heart Association · 2022Article
- Rho Kinases in Embryonic Development and Stem Cell Research.Archivum immunologiae et therapiae experimentalis · 2022Review
- Inhibition of mitochondrial respiration has fundamentally different effects on proliferation, cell survival and stress response in immature versus differentiated cardiomyocyte cell lines.Frontiers in cell and developmental biology · 2022Article
- Protective effect of oleuropein on ketamine-induced cardiotoxicity in rats.Naunyn-Schmiedeberg's archives of pharmacology · 2020Article
- ROCK2 inhibition enhances the thermogenic program in white and brown fat tissue in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Doxorubicin-induced cardiotoxicity is maturation dependent due to the shift from topoisomerase IIα to IIβ in human stem cell derived cardiomyocytes.Journal of cellular and molecular medicine · 2019Article
- Disruption of both ROCK1 and ROCK2 genes in cardiomyocytes promotes autophagy and reduces cardiac fibrosis during aging.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Clinical and preclinical evidence of sex-related differences in anthracycline-induced cardiotoxicity.Biology of sex differences · 2018Review
- Disruption of ROCK1 gene restores autophagic flux and mitigates doxorubicin-induced cardiotoxicity.Oncotarget · 2018Article
- Doxorubicin-induced chronic dilated cardiomyopathy-the apoptosis hypothesis revisited.Journal of molecular medicine (Berlin, Germany) · 2017Review
- Developmental Regulation of Mitochondrial Apoptosis by c-Myc Governs Age- and Tissue-Specific Sensitivity to Cancer Therapeutics.Cancer cell · 2017Article
- Dissecting the Mechanisms of Doxorubicin and Oxidative Stress-Induced Cytotoxicity: The Involvement of Actin Cytoskeleton and ROCK1.PloS one · 2015Article
- ROCK1 deficiency enhances protective effects of antioxidants against apoptosis and cell detachment.PloS one · 2014Article
- Traditional and novel methods to assess and prevent chemotherapy-related cardiac dysfunction noninvasively.Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology · 2013Review
- Distinct roles for ROCK1 and ROCK2 in the regulation of cell detachment.Cell death & disease · 2013Article
- QiShenYiQi Pills, a Compound Chinese Medicine, Ameliorates Doxorubicin-Induced Myocardial Structure Damage and Cardiac Dysfunction in Rats.Evidence-based complementary and alternative medicine : eCAM · 2013Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Doxorubicin is a highly effective chemotherapeutic agent used for treating a wide spectrum of tumors, but its usage is limited because of its dose-dependent cardiotoxicity, especially in pediatric patients. Accumulating evidence indicates that caspase-dependent apoptosis contributes to the cardiotoxicity of doxorubicin. However, less attention has been paid to the effects of age on doxorubicin-induced apoptosis signaling in myocardium. This study focused on investigating differential apoptotic sensitivity between neonatal and adult myocardium, in particular, between neonatal and adult cardiomyocytes in vivo. Our results show that caspase-3 activity in normal mouse hearts decreased by ≥ 20-fold within the first 3 wk after birth, associated with a rapid downregulation in the expression of key proapoptotic proteins in intrinsic and extrinsic pathways. This rapid downregulation of caspase-3 activity was confirmed by immunostaining for cleaved caspase-3 and terminal deoxynucleotidyl transferase dUTP-mediated nick-end label staining. Doxorubicin treatment induced a dose-dependent increase in caspase-3 activity and apoptosis in neonatal mouse hearts, and both caspase-8 and caspase-9 activations were involved. Using transgenic mice with a nuclear localized LacZ reporter gene to label cardiomyocytes in vivo, we observed a fourfold higher level of doxorubicin-induced cardiomyocyte apoptosis in 1-wk-old mice compared with that in 3-wk-old mice. This study points to a major difference in apoptotic signaling in doxorubicin cardiotoxicity between neonatal and adult mouse hearts and reveals a critical transition from high to low susceptibility to doxorubicin-induced apoptosis during postnatal heart maturation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.