ArticleJournal of cellular and molecular medicine
Distinct mechanisms of cardiomyocyte apoptosis induced by doxorubicin and hypoxia converge on mitochondria and are inhibited by Bcl-xL.
Article in Journal of cellular and molecular medicine. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 88 citations in OpenAlex.
- Unveiling the Complexities: Exploring Mechanisms of Anthracyclineinduced Cardiotoxicity.Current cardiology reviews · 2025Review
- The protective effect of the mitochondrial-derived peptide MOTS-c on LPS-induced septic cardiomyopathy.Acta biochimica et biophysica Sinica · 2023Article
- CD47 antibody protects mice from doxorubicin-induced myocardial damage by suppressing cardiomyocyte apoptosis.Experimental and therapeutic medicine · 2022Article
- Choline Protects the Heart from Doxorubicin-Induced Cardiotoxicity through Vagal Activation and Nrf2/HO-1 Pathway.Oxidative medicine and cellular longevity · 2022Article
- Histone methyltransferase KMT2D contributes to the protection of myocardial ischemic injury.Frontiers in cell and developmental biology · 2022Article
- Endogenous Hydrogen Sulfide Persulfidates Caspase-3 at Cysteine 163 to Inhibit Doxorubicin-Induced Cardiomyocyte Apoptosis.Oxidative medicine and cellular longevity · 2022Article
- Could curcumin ameliorate titanium dioxide nanoparticles effect on the heart? A histopathological, immunohistochemical, and genotoxic study.Environmental science and pollution research international · 2019Article
- Liraglutide ameliorates cardiotoxicity induced by doxorubicin in rats through the Akt/GSK-3β signaling pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2017Article
- Beet root juice protects against doxorubicin toxicity in cardiomyocytes while enhancing apoptosis in breast cancer cells.Molecular and cellular biochemistry · 2016Article
- Cardioprotective effects of sitagliptin against doxorubicin-induced cardiotoxicity in rats.Experimental biology and medicine (Maywood, N.J.) · 2016Article
- Curcumin Downregulates Phosphate Carrier and Protects against Doxorubicin Induced Cardiomyocyte Apoptosis.BioMed research international · 2016Article
- Epac is required for GLP-1R-mediated inhibition of oxidative stress and apoptosis in cardiomyocytes.Molecular endocrinology (Baltimore, Md.) · 2015Article
- Oral treatment with the herbal formula B307 alleviates cardiac toxicity in doxorubicin-treated mice via suppressing oxidative stress, inflammation, and apoptosis.OncoTargets and therapy · 2015Article
- Cardiomyocyte-specific role of miR-24 in promoting cell survival.Journal of cellular and molecular medicine · 2015Article
- MicroRNA-208a Silencing Attenuates Doxorubicin Induced Myocyte Apoptosis and Cardiac Dysfunction.Oxidative medicine and cellular longevity · 2015Article
- Nanocurcumin Prevents Hypoxia Induced Stress in Primary Human Ventricular Cardiomyocytes by Maintaining Mitochondrial Homeostasis.PloS one · 2015Article
- TanshinoneIIA and cryptotanshinone protect against hypoxia-induced mitochondrial apoptosis in H9c2 cells.PloS one · 2013Article
- Hydrogen sulfide protects H9c2 cells against doxorubicin-induced cardiotoxicity through inhibition of endoplasmic reticulum stress.Molecular and cellular biochemistry · 2012Article
- Article
- Mitochondria death/survival signaling pathways in cardiotoxicity induced by anthracyclines and anticancer-targeted therapies.Biochemistry research international · 2012Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypoxia and doxorubicin can cause cardiotoxicity and loss of myocardial function. These effects are due, in part, to an induction of apoptosis. Herein we identify the apoptotic pathways activated in H9c2 cells in response to hypoxia (O(2)/N(2)/CO(2), 0.5:94.5:5) and doxorubicin (0.5 muM). Although the apoptosis induced was accompanied by induction of Fas and Fas ligand, the death receptor pathway was not critical for caspase activation by either stimulus. Hypoxia induced the expression of endoplasmic reticulum (ER) stress mediators and processed ER-resident pro-caspase-12 whereas doxorubicin did not induce an ER stress response. Most importantly, both stimuli converged on mitochondria to promote apoptosis. Accumulation of cytochrome c in the cytosol coincided with the processing of pro-caspase-9 and -3. Increasing the expression of the anti-apoptotic protein Bcl-x(L), either by dexamethasone or adenovirus-mediated transduction, protected H9c2 cells from doxorubicin- and hypoxia-induced apoptosis. Bcl-x(L) attenuated mitochondrial cytochrome crelease and reduced downstream pro-caspase processing and apoptosis. These data demonstrate that two distinct cardiomyocyte-damaging stimuli converge on mitochondria thus presenting this organelle as a potentially important therapeutic target for anti-apoptotic strategies for cardiovascular diseases.
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