ReviewCardiovascular toxicology2021
Mitochondrial Sirtuins and Doxorubicin-induced Cardiotoxicity.
Review in Cardiovascular toxicology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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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.
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Who cites it
26 citing papers in PubMed, 58 citations in OpenAlex.
- Mitochondrial quality control in health and disease: Updates 2026.Chinese medical journal · 2026Review
- Shikonin attenuates doxorubicin-induced myocardial senescence and fibrosis in association with improved redox and mitochondrial homeostasis.Molecular biology reports · 2026Article
- Chemo-/radiotherapy-induced cardiomyopathy: roles of mitochondria and endoplasmic reticulum.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2026Review
- Mitochondrial Dysfunction in Cardiac Diseases: Insights into Pathophysiology and Clinical Outcomes.Current cardiology reviews · 2026Review
- Mechanisms and the Role of p38 MAPK Signaling in Doxorubicin-Induced Cardiotoxicity: A Review.International journal of general medicine · 2026Review
- Article
- Diminazine protects against cardiac aging through the improvement of mitophagy and apoptosis in aging rats induced by D-galactose.BMC cardiovascular disorders · 2025Article
- Cardioprotection strategies for anthracycline cardiotoxicity.Basic research in cardiology · 2025Review
- Identification of Dalbergiae Odoriferae Lignum active ingredients and potential mechanisms in the treatment of adriamycin-induced cardiotoxicity based on network pharmacology and experimental verification.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Role of Oxidative Stress and Inflammation in Doxorubicin-Induced Cardiotoxicity: A Brief Account.International journal of molecular sciences · 2024Review
- Eupatilin attenuates doxorubicin-induced cardiotoxicity by activating the PI3K-AKT signaling pathway in mice.Molecular and cellular biochemistry · 2024Article
- Sirtuin 4 (Sirt4) downregulation contributes to chondrocyte senescence and osteoarthritis via mediating mitochondrial dysfunction.International journal of biological sciences · 2024Article
- The Distant Molecular Effects on the Brain by Cancer Treatment.Brain sciences · 2023Article
- Article
- Mitochondria and Brain Disease: A Comprehensive Review of Pathological Mechanisms and Therapeutic Opportunities.Biomedicines · 2023Review
- SIRT4 in ageing.Biogerontology · 2023Review
- Targeting Energy Protection as a Novel Strategy to Disclose Di'ao Xinxuekang against the Cardiotoxicity Caused by Doxorubicin.International journal of molecular sciences · 2023Article
- Research progress of AMP-activated protein kinase and cardiac aging.Open life sciences · 2023Review
- miR-16-5p Regulates Ferroptosis by Targeting SLC7A11 in Adriamycin-Induced Ferroptosis in Cardiomyocytes.Journal of inflammation research · 2023Article
- Protective Effects ofMolecules (Basel, Switzerland) · 2022Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Doxorubicin (DOX) is the most effective and extensively used treatment for many tumors. However, its clinical use is hampered by its cardiotoxicity. DOX-induced mitochondrial dysfunction, which causes reactive oxygen species (ROS) generation, cardiomyocyte death, bioenergetic failure, and decreased cardiac function, is a very important mechanism of cardiotoxicity. These cellular processes are all linked by mitochondrial sirtuins (SIRT3-SIRT4). Mitochondrial sirtuins preserve mitochondrial function by increasing mitochondrial metabolism, inhibiting ROS generation by activating the antioxidant enzyme manganese-dependent superoxide dismutase (MnSOD), decreasing apoptosis by activating the forkhead homeobox type O (FOXO) and P53 pathways, and increasing autophagy through AMP-activated protein kinase (AMPK)/mTOR signaling. Thus, sirtuins function at the control point of many mechanisms involved in DOX-induced cardiotoxicity. In this review, we focus on the role of mitochondrial sirtuins in mitochondrial biology and DOX-induced cardiotoxicity. A further aim is to highlight other mitochondrial processes, such as autophagy (mitophagy) and mitochondrial quality control (MQC), for which the effect of mitochondrial sirtuins on cardiotoxicity is unknown.
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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.