ArticleAmerican journal of translational research2017
Sirt3 attenuates doxorubicin-induced cardiac hypertrophy and mitochondrial dysfunction via suppression of Bnip3.
Article in American journal of translational research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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Who cites it
35 citing papers in PubMed, 62 citations in OpenAlex.
- Novel Mechanism of and Therapeutic Approach for Anthracycline-Induced Cardiotoxicity.Cancer research communications · 2026Article
- Dapagliflozin Protects Cardiomyocytes against Doxorubicin-Induced Toxicity by Modulating Sirtuin 1/Sirtuin 3 and Ferroptosis Pathway.ACS pharmacology & translational science · 2026Article
- RNAi-mediated p38δ silencing mitigates anthracycline cardiotoxicity in female mice.American journal of physiology. Heart and circulatory physiology · 2026Article
- TAX1BP1 protects against doxorubicin-induced cardiotoxicity via maintaining mitochondrial function in a mTORC2-SGK1-VDAC1 manner.Molecular medicine (Cambridge, Mass.) · 2026Article
- Chemo-/radiotherapy-induced cardiomyopathy: roles of mitochondria and endoplasmic reticulum.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2026Review
- Review
- Cardiomyocyte specific CD38 deletion protects heart from acute myocardial infarction by activating Sirt3 signaling pathway.Scientific reports · 2025Article
- Circ-0006332 stimulates cardiomyocyte pyroptosis via the miR-143/TLR2 axis to promote doxorubicin-induced cardiac damage.Epigenetics · 2024Article
- TongGuanWan Alleviates Doxorubicin- and Isoproterenol-Induced Cardiac Hypertrophy and Fibrosis by Modulating Apoptotic and Fibrotic Pathways.International journal of molecular sciences · 2024Article
- Targeting SIRT2 in Aging-Associated Fibrosis Pathophysiology.Aging and disease · 2024Review
- A review of the pathophysiological mechanisms of doxorubicin-induced cardiotoxicity and aging.npj aging · 2024Review
- Reduction of Doxorubicin-Induced Cardiotoxicity by Co-Administration of Smart Liposomal Doxorubicin and Free Quercetin: In Vitro and In Vivo Studies.Pharmaceutics · 2023Article
- Electrocardiographic and biochemical analysis of anthracycline induced cardiotoxicity in breast cancer patients from Southern Sri Lanka.BMC cancer · 2023Article
- Investigating Physiopathological Roles for Sirtuins in a Mouse Model.Methods in molecular biology (Clifton, N.J.) · 2023Article
- A Glb1-2A-mCherry reporter monitors systemic aging and predicts lifespan in middle-aged mice.Nature communications · 2022Article
- SUMOylation targeting mitophagy in cardiovascular diseases.Journal of molecular medicine (Berlin, Germany) · 2022Review
- Review
- The Role of Mitochondrial Quality Control in Anthracycline-Induced Cardiotoxicity: From Bench to Bedside.Oxidative medicine and cellular longevity · 2022Review
- Mitochondrial sirtuin 3 and various cell death modalities.Frontiers in cell and developmental biology · 2022Review
- MicroRNAs in doxorubicin-induced cardiotoxicity: The DNA damage response.Frontiers in pharmacology · 2022Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Doxorubicin (Dox) is an anthracycline antibiotic widely used in cancer treatment. Although its antitumor efficacy appears to be dose dependent, its clinical use is greatly restricted by development of cardiotoxicity. Sirtuin-3 (Sirt3) is the major deacetylase within the mitochondrial matrix that plays an important role in regulation of cardiac function. This study was performed to identify the regulatory role of Sirt3 on Dox-induced cardiac hypertrophy and mitochondrial dysfunction in rats in vivo and in vitro. We found that adenovirus-mediated overexpression of Sirt3 resulted in marked inhibition of Dox-induced cardiac hypertrophy, particularly mitochondrial dysfunction including opening of the mitochondrial permeability transition pore (mPTP), loss of mitochondrial membrane potential (ΔΨm), respiration dysfunction, and mitochondrial reactive oxygen species (ROS) production. Further study revealed that Bcl-2-like 19 kDa-interacting protein 3 (Bnip3) mRNA and protein expression levels were altered in cardiomyocytes in vivo and in vitro after Dox treatment, and these increases were significantly inhibited by Sirt3 overexpression. Interestingly, the Dox-disrupted mitochondrial Cox1-Ucp3 complexes were preserved by Sirt3 overexpression. Finally, recombinant adeno-associated virus-mediated overexpression of Bnip3 (AAV-Bnip3) in rat hearts and cardiomyocytes completely impaired the protective effects of Sirt3 on Dox-induced cardiac toxicity and mitochondrial dysfunction. These findings reveal a new molecular mechanism in which Sirt3 restores mitochondrial respiratory chain defects, and cell viability of Dox-damaged cardiomyocytes is mutually dependent on and obligatorily linked to suppression of Bnip3 gene expression. Interventions that antagonize Bnip3 may contribute to the beneficial effect of Sirt3 regarding prevention of mitochondrial injury and heart failure in cancer patients undergoing chemotherapy.
Indexed as
Identifiers
28804553PMC5553885W2746904443What 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.