ArticleAntioxidants (Basel, Switzerland)2023
PGC-1α Agonist Rescues Doxorubicin-Induced Cardiomyopathy by Mitigating the Oxidative Stress and Necroptosis.
Article in Antioxidants (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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.
The trial behind it
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Who cites it
18 citing papers in PubMed, 22 citations in OpenAlex.
- GIPC1 governed ferroptosis by regulating DECR1-modulating lipid homeostasis during dilated cardiomyopathy (DCM).Cell death and differentiation · 2026Article
- [Lonicera japonica attenuates oxidative stress and improves post-ischemic heart failure in miceNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Mitochondrial Dysfunction at the Crossroads of Necroptosis: Mechanisms, Molecular Mediators, and Therapeutic Opportunities.Journal of cellular and molecular medicine · 2026Review
- Lgr6Genes & diseases · 2026Review
- Molecular regulation of PGC-1α: from protein-protein interactions and post-translational modifications to pharmacological modulation.Journal of molecular medicine (Berlin, Germany) · 2026Review
- Cardiomyocyte programmed cell death in dilated cardiomyopathy: molecular crosstalk and therapeutic implications.Frontiers in cell and developmental biology · 2026Review
- Mitochondrial dysfunction-driven PANoptosis in doxorubicin-induced cardiotoxicity: mechanistic insights and intervention strategies.Frontiers in pharmacology · 2026Review
- M6a demethylase FTO regulates the oxidative stress, mitochondrial biogenesis of cardiomyocytes and PGC-1a stability in myocardial ischemia-reperfusion injury.Redox report : communications in free radical research · 2025Article
- Role of the AMPK/PGC-1α/SIRT3-Mediated Mitochondrial Dysfunction in the Neurotoxicity of Methanol.Molecular neurobiology · 2025Article
- AMPK/SIRT1/PGC-1α Signaling Pathway: Molecular Mechanisms and Targeted Strategies From Energy Homeostasis Regulation to Disease Therapy.CNS neuroscience & therapeutics · 2025Review
- CD4International journal of molecular sciences · 2025Article
- PGC1α regulates the mitochondrial metabolism response to cyclic stretch, which inhibits neointimal hyperplasia.Cellular and molecular life sciences : CMLS · 2025Article
- Cardiomyopathies and a brief insight into DOX-induced cardiomyopathy.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2025Review
- Bioinformatics analyses reveal the autophagy-related feature biomarkers in dilated cardiomyopathy with heart failure.Frontiers in cardiovascular medicine · 2025Article
- New insights into mitochondrial quality control in anthracycline-induced cardiotoxicity: molecular mechanisms, therapeutic targets, and natural products.International journal of biological sciences · 2025Review
- Article
- The mechanism and therapeutic strategies in doxorubicin-induced cardiotoxicity: Role of programmed cell death.Cell stress & chaperones · 2024Review
- Swimming Exercise Attenuates DOX-Induced Cardiotoxicity by Modulating Apoptosis and DRP1/PGC1α/miR-23a Dependent Pathway in Rat Heart Tissue.Avicenna journal of medical biotechnologyArticle
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiomyopathy (particularly dilated cardiomyopathy (DCM)) significantly contributes to development and progression of heart failure (HF), and inflammatory factors further deteriorate the symptoms. Morphological and functional defects of the heart in doxorubicin (DOX)-induced cardiomyopathy (cardiotoxicity) are similar to those of DCM. We used anagonist of PGC-1α (PPAR (peroxisome proliferator-activated receptor-gamma)-γ coactivator-1α) that is considered as the 'master regulator' of mitochondrial biogenesis with an aim to rescue the DOX-induced deleterious effects on the heart. Forty male C57BL/6J mice (8 weeks old) were divided in four groups, Control, DOX, ZLN005, and ZLN005 + DOX (
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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.