ArticleMolecules (Basel, Switzerland)2021
Cryptotanshinone Ameliorates Doxorubicin-Induced Cardiotoxicity by Targeting Akt-GSK-3β-mPTP Pathway In Vitro.
Article in Molecules (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Effects of cryptotanshinone in treatment of polycystic ovary syndrome in rats: a systematic review and meta-analysis.Frontiers in pharmacology · 2025Pooled it
- Recent Advances in Understanding the Mechanisms of Therapy-Related Cardiovascular Events in Pediatric Hematologic Malignancies.Reviews in cardiovascular medicine · 2026Review
- TAX1BP1 protects against doxorubicin-induced cardiotoxicity via maintaining mitochondrial function in a mTORC2-SGK1-VDAC1 manner.Molecular medicine (Cambridge, Mass.) · 2026Article
- Protective effect of Lonicerae Japonicae Flos extract against doxorubicin-induced myocardial injury in mice and the possible mechanisms.Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- FOXO1-NMNAT3 axis dysregulation promotes doxorubicin cardiotoxicity: NADRedox report : communications in free radical research · 2025Article
- Advances in pharmacological research on myocardial remodeling agents: A decade in review.Medicine · 2025Review
- NADPH Oxidases in Cancer Therapy-Induced Cardiotoxicity: Mechanisms and Therapeutic Approaches.Cardiovascular toxicology · 2025Review
- Small Molecules Targeting Mitochondria: A Mechanistic Approach to Combating Doxorubicin-Induced Cardiotoxicity.Cardiovascular toxicology · 2025Review
- Natural Products From Traditional Chinese Medicine: Potential Therapeutic Agents in Cancer Therapy-Induced Cardiotoxicity.Drug design, development and therapy · 2025Review
- Unveiling the Complexities: Exploring Mechanisms of Anthracyclineinduced Cardiotoxicity.Current cardiology reviews · 2025Review
- eEF2K alleviates doxorubicin-induced cardiotoxicity by inhibiting GSK3β and improving autophagy dysfunction.Cell biology and toxicology · 2024Article
- Meldonium, as a potential neuroprotective agent, promotes neuronal survival by protecting mitochondria in cerebral ischemia-reperfusion injury.Journal of translational medicine · 2024Article
- Inhibition of mitochondrial cyclophilin D, a downstream target of glycogen synthase kinase 3α, improves sperm motility.Reproductive biology and endocrinology : RB&E · 2024Article
- Oxyphenbutazone ameliorates carfilzomib induced cardiotoxicity in rats via inhibition of oxidative free radical burst and NF-κB/IκB-α pathway.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2024Article
- Metformin reverses oxidative stress‑induced mitochondrial dysfunction in pre‑osteoblasts via the EGFR/GSK‑3β/calcium pathway.International journal of molecular medicine · 2023Article
- Potential chemoprotective effects of active ingredients inFrontiers in cardiovascular medicine · 2023Review
- Effects ofFrontiers in cell and developmental biology · 2023Review
- Cationic antimicrobial peptide NRC-03 induces oral squamous cell carcinoma cell apoptosis via CypD-mPTP axis-mediated mitochondrial oxidative stress.Redox biology · 2022Article
- Akt-GSK3β-mPTP pathway regulates the mitochondrial dysfunction contributing to odontoblasts apoptosis induced by glucose oxidative stress.Cell death discovery · 2022Article
- Ticagrelor reduces doxorubicin-induced pyroptosis of rat cardiomyocytes by targeting GSK-3β/caspase-1.Frontiers in cardiovascular medicine · 2022Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Cardiotoxicity is one of the main side effects of doxorubicin (Dox) treatment. Dox could induce oxidative stress, leading to an opening of the mitochondrial permeability transition pore (mPTP) and apoptosis in cardiomyocytes. Previous studies have shown that Cryptotanshinone (Cts) has potential cardioprotective effects, but its role in Dox-induced cardiotoxicity (DIC) remains unknown. A Dox-stimulated H9C2 cell model was established. The effects of Cts on cell viability, reactive oxygen species (ROS), superoxide ion accumulation, apoptosis and mitochondrial membrane potential (MMP) were evaluated. Expressions of proteins in Akt-GSK-3β pathway were detected by Western blot. An Akt inhibitor was applied to investigate the effects of Cts on the Akt-GSK-3β pathway. The effects of Cts on the binding of p-GSK-3β to ANT and the formation of the ANT-CypD complex were explored by immunoprecipitation assay. The results showed that Cts could increase cell viability, reduce ROS levels, inhibit apoptosis and protect mitochondrial membrane integrity. Cts increased phosphorylated levels of Akt and GSK-3β. After cells were co-treated with an Akt inhibitor, the effects of Cts were abolished. An immunoprecipitation assay showed that Cts significantly increased GSK-3β-ANT interaction and attenuated Dox-induced formation of the ANT-CypD complex, thereby inhibiting opening of the mPTP. In conclusion, Cts could ameliorate oxidative stress and apoptosis via the Akt-GSK-3β-mPTP pathway.
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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.