ArticleInternational journal of clinical and experimental pathology2015
Effects of PPARα/PGC-1α on the energy metabolism remodeling and apoptosis in the doxorubicin induced mice cardiomyocytes in vitro.
Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 40 citations in OpenAlex.
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- Streptozotocin-induced hyperglycemia unmasks cardiotoxicity induced by doxorubicin.Scientific reports · 2025Article
- MicroRNA‑378: An important player in cardiovascular diseases (Review).Molecular medicine reports · 2023Review
- Peroxisome proliferator-activated receptor-α (PPARα) regulates wound healing and mitochondrial metabolism in the cornea.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Identification of shared fatty acid metabolism related signatures in dilated cardiomyopathy and myocardial infarction.Future science OA · 2023Article
- Cardiotoxicity of anti-cancer drugs: cellular mechanisms and clinical implications.Frontiers in cardiovascular medicine · 2023Review
- Synergistic Effects of Ginsenoside Rb3 and Ferruginol in Ischemia-Induced Myocardial Infarction.International journal of molecular sciences · 2022Article
- The Employment of GeneraNutrients · 2022Review
- Pharmacological effects of higenamine based on signalling pathways and mechanism of action.Frontiers in pharmacology · 2022Review
- The Role of Mitochondrial Quality Control in Anthracycline-Induced Cardiotoxicity: From Bench to Bedside.Oxidative medicine and cellular longevity · 2022Review
- Chemotherapy-induced Cardiac18F-FDG Uptake in Patients with Lymphoma: An Early Metabolic Index of Cardiotoxicity?Arquivos brasileiros de cardiologia · 2022Article
- A lack of ChREBP inhibits mitochondrial cristae formation in brown adipose tissue.Molecular and cellular biochemistry · 2021Article
- Metabolomics coupled with integrated approaches reveal the therapeutic effects of higenamine combined with [6]-gingerol on doxorubicin-induced chronic heart failure in rats.Chinese medicine · 2020Article
- Mitochondrial Determinants of Doxorubicin-Induced Cardiomyopathy.Circulation research · 2020Review
- The Essential Oil from Acori Tatarinowii Rhizome (the Dried Rhizome ofEvidence-based complementary and alternative medicine : eCAM · 2020Article
- Qishen granules exerts cardioprotective effects on rats with heart failure via regulating fatty acid and glucose metabolism.Chinese medicine · 2020Article
- Crim1 suppresses left ventricular hypertrophy.Biomedical reports · 2019Article
- Keeping the Heart Fitm2 during Chemotherapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2019Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dilated cardiomyopathy is the most frequent form of myocardial disease. Many factors contribute to dilated cardiomyopathy, for instance, long-term use of doxorubicin, one of the anthracyclines clinically used for cancer chemotherapy, result in dilated cardiomyopathy and congestive heart failure. However, the mechanism underlining doxorubicin-induced cardiomyocyte is still not fully understood. In this study, we evaluate the effects and their mechanisms of PPARα and PGC-1α pathways in doxorubicin induced mice cardiomyocytes. In vitro, cardiomyocytes isolated from hearts of adult FVB/NJ mice were treated with doxorubicin, GW 6471 (PPARα inhibitors) and WY14643 (PPARα agonists). The expression of PPARα and PGC-1α were detected via western blotting and Quantitative Real-Time PCR methods. Changes in energy and substrate metabolism were analyzed. MTT and flow cytometry were used for cell proliferation and apoptosis analysis. We detected expression of PPARα and PGC-1α was significantly higher in control group than doxorubicin group. Mitochondrial dysfunction was found in doxorubicin group including lower content of high-energy phosphates, significantly decreased mitochondrial ANT transport activity and markedly reduced mitochondrial membrane potential compared with control group. Metabolic remodeling existed in doxorubicin group because of higher concentration of free fatty acid and glucose consumption than of control group. More accumulations of reactive oxygen species were detected in doxorubicin group. The decreased cell viability and increased cell apoptosis observed in doxorubicin group. Severe apoptosis in doxorubicin group was verified by a set of markers including Bax, Bcl-2, cytosolic cytochrome c and caspase-3 up-regulation expression. These findings indicate that the PPARα and PGC-1α are closely involved in energy metabolism remodeling and apoptosis in cardiomyocytes.
Indexed as
Identifiers
26722406PMC4680351W2418228349What OpenQuestion holds
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.