ArticleFree radical biology & medicine2014
Redox proteomic identification of HNE-bound mitochondrial proteins in cardiac tissues reveals a systemic effect on energy metabolism after doxorubicin treatment.
Article in Free radical biology & medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 106 citations in OpenAlex.
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- Facts, Dogmas, and Unknowns About Mitochondrial Reactive Oxygen Species in Cancer.Antioxidants (Basel, Switzerland) · 2024Review
- Oxidative stress is two-sided in the treatment of acute myeloid leukemia.Cancer medicine · 2024Review
- Shikonin alleviates doxorubicin-induced cardiotoxicity via Mst1/Nrf2 pathway in mice.Scientific reports · 2024Article
- The Distant Molecular Effects on the Brain by Cancer Treatment.Brain sciences · 2023Article
- A common East-Asian ALDH2 mutation causes metabolic disorders and the therapeutic effect of ALDH2 activators.Nature communications · 2023Article
- α-Bisabolol, a Dietary Sesquiterpene, Attenuates Doxorubicin-Induced Acute Cardiotoxicity in Rats by Inhibiting Cellular Signaling Pathways, Nrf2/Keap-1/HO-1, Akt/mTOR/GSK-3β, NF-κB/p38/MAPK, and NLRP3 Inflammasomes Regulating Oxidative Stress and Inflammatory Cascades.International journal of molecular sciences · 2023Article
- The 4-Hydroxynonenal-Protein Adducts and Their Biological Relevance: Are Some Proteins Preferred Targets?Antioxidants (Basel, Switzerland) · 2023Review
- Electrophilic Aldehyde 4-Hydroxy-2-Nonenal Mediated Signaling and Mitochondrial Dysfunction.Biomolecules · 2022Review
- Extracellular Vesicles and Cancer Therapy: Insights into the Role of Oxidative Stress.Antioxidants (Basel, Switzerland) · 2022Review
- Altered Metabolism in Alzheimer Disease Brain: Role of Oxidative Stress.Antioxidants & redox signaling · 2022Review
- Male Infertility and Oxidative Stress: A Focus on the Underlying Mechanisms.Antioxidants (Basel, Switzerland) · 2022Review
- The Potential Role of Mitochondrial Acetaldehyde Dehydrogenase 2 in Urological Cancers From the Perspective of Ferroptosis and Cellular Senescence.Frontiers in cell and developmental biology · 2022Review
- Mitochondrial dysfunction in skeletal muscle contributes to the development of acute insulin resistance in mice.Journal of cachexia, sarcopenia and muscle · 2021Article
- Protein Carbonylation: Emerging Roles in Plant Redox Biology and Future Prospects.Plants (Basel, Switzerland) · 2021Review
- Uncoupling proteins in the mitochondrial defense against oxidative stress.Progress in retinal and eye research · 2021Review
- 4HNE Impairs Myocardial Bioenergetics in Congenital Heart Disease-Induced Right Ventricular Failure.Circulation · 2020Article
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
Abstract
Doxorubicin (DOX), one of the most effective anticancer drugs, is known to generate progressive cardiac damage, which is due, in part, to DOX-induced reactive oxygen species (ROS). The elevated ROS often induce oxidative protein modifications that result in alteration of protein functions. This study demonstrates that the level of proteins adducted by 4-hydroxy-2-nonenal (HNE), a lipid peroxidation product, is significantly increased in mouse heart mitochondria after DOX treatment. A redox proteomics method involving two-dimensional electrophoresis followed by mass spectrometry and investigation of protein databases identified several HNE-modified mitochondrial proteins, which were verified by HNE-specific immunoprecipitation in cardiac mitochondria from the DOX-treated mice. The majority of the identified proteins are related to mitochondrial energy metabolism. These include proteins in the citric acid cycle and electron transport chain. The enzymatic activities of the HNE-adducted proteins were significantly reduced in DOX-treated mice. Consistent with the decline in the function of the HNE-adducted proteins, the respiratory function of cardiac mitochondria as determined by oxygen consumption rate was also significantly reduced after DOX treatment. Treatment with Mn(III) meso-tetrakis(N-n-butoxyethylpyridinium-2-yl)porphyrin, an SOD mimic, averted the doxorubicin-induced mitochondrial dysfunctions as well as the HNE-protein adductions. Together, the results demonstrate that free radical-mediated alteration of energy metabolism is an important mechanism mediating DOX-induced cardiac injury, suggesting that metabolic intervention may represent a novel approach to preventing cardiac injury after chemotherapy.
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