ArticleCardiovascular therapeutics2022
Protective Effect of Qiliqiangxin against Doxorubicin-Induced Cardiomyopathy by Suppressing Excessive Autophagy and Apoptosis.
Article in Cardiovascular therapeutics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- The Role of mTOR in the Doxorubicin-Induced Cardiotoxicity: A Systematic Review.Cell biochemistry and biophysics · 2025Pooled it
- Autophagic therapeutic targeting for Doxorubicin-induced cardiomyopathy.Molecular biology reports · 2026Review
- Integrating Network Pharmacology and In Vitro 3D Cardiac Organoid Model Validation to Investigate the Action Mechanism of Shenfu Xiangshao Decoction on Heart Failure.Journal of cardiovascular pharmacology · 2026Article
- Doxorubicin-Induced Cardiac Remodeling: Mechanisms and Mitigation Strategies.Cardiovascular drugs and therapy · 2026Review
- Qiliqiangxin capsule attenuates platelet activation and thrombosis by suppressing CaThrombosis journal · 2026Article
- Article
- Traditional Chinese medicine as a protective strategy against chemotherapy-induced cardiotoxicity: An overview of the literature.Journal of traditional and complementary medicine · 2025Review
- Protective effects of lemon and orange peels and olive oil on doxorubicin-induced myocardial damage via inhibition of oxidative stress and inflammation pathways.Frontiers in pharmacology · 2025Article
- Effects of Glutamine or Glucose Deprivation on Inflammation and Tight Junction Disruption in Yak Rumen Epithelial Cells.Animals : an open access journal from MDPI · 2024Article
- Chinese and western medicine treatment of myocardial fibrosis drugs.Frontiers in cardiovascular medicine · 2024Review
- Qili Qiangxin capsule attenuates myocardial fibrosis by modulating collagen homeostasis post-infarction in rats.PloS one · 2024Article
- Recent Advances in the Mechanisms of Cell Death and Dysfunction in Doxorubicin Cardiotoxicity.Reviews in cardiovascular medicine · 2023Review
- Review
- Rifampicin efficacy against doxorubicin-induced cardiotoxicity in mice.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2023Article
- M2b macrophages protect against doxorubicin induced cardiotoxicity via alternating autophagy in cardiomyocytes.PloS one · 2023Article
- Emerging roles of ferroptosis in cardiovascular diseases.Cell death discovery · 2022Review
- Qiliqiangxin Capsule Modulates Calcium Transients and Calcium Sparks in Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Role and molecular mechanism of traditional Chinese medicine in preventing cardiotoxicity associated with chemoradiotherapy.Frontiers in cardiovascular medicine · 2022Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDoxorubicin (DOX) is one of the most potent and widely prescribed antitumor agents; however, its clinical use is limited by cardiac side effects. In this study, we aimed to clarify the protective effects of Qiliqiangxin (QL), a traditional Chinese medicine formulation, on DOX-induced cardiotoxicity and to explore the underlying mechanisms in a rat model.
methodsMale Sprague-Dawley rats were randomly assigned to three groups with different interventions (control, DOX, and DOX plus QL) for 31 days. Cardiac function was monitored. The levels of oxidative stress in plasm were detected, the activities of autophagy and apoptosis in rat hearts were determined, and then, the related PI3K/AKT/mTOR signal pathway regulating apoptosis and autophagy was investigated.
resultsQL improved cardiac dysfunction and decreased the increased level of cardiac enzymes in plasm caused by DOX. Moreover, DOX exposure resulted in oxidative stress enhancement, which was suppressed by QL treatment. Then, we discovered that DOX intervention caused the apoptosis of cardiomyocytes by activating the mitochondrial-dependent apoptotic pathway which was strongly inhibited by QL treatment. Furthermore, there was a significant increase in autophagic activities in the DOX-stimulated myocardium. Administration of QL substantially inhibited the enhanced autophagic activities, which might be attributed to the activation of PI3K/AKT/mTOR cascade, followed by suppression of ULK1 activity.
conclusionsQL exhibited protective roles against DOX-induced cardiotoxicity possibly via mediating the PI3K/AKT/mTOR pathway, leading to inhibition of autophagy and subsequent apoptosis activities.
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