ArticleFrontiers in cardiovascular medicine2021
Periplocymarin Alleviates Doxorubicin-Induced Heart Failure and Excessive Accumulation of Ceramides.
Article in Frontiers in cardiovascular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- A narrative review of metabolomics approaches in identifying biomarkers of doxorubicin-induced cardiotoxicity.Metabolomics : Official journal of the Metabolomic Society · 2025Pooled it
- Xijiaqi Formula attenuates myocardial infarction-induced chronic heart failure by inhibiting TGF-β1/Smads-mediated fibroblast activation.Pharmaceutical biology · 2026Article
- Diagnostic Ion-Guided Isolation and Characterization of Trace Periplocin-Derived Cardenolide Metabolites from Rat Urine.Molecules (Basel, Switzerland) · 2026Article
- MARCH2 prevents doxorubicin-induced cardiomyopathy by stabilizing NR1H2 and promoting clearance of apoptotic cardiomyocytes.Nature communications · 2026Article
- Cardiotoxicity induced by traditional chemotherapy: mechanisms and mitigation strategies.Apoptosis : an international journal on programmed cell death · 2026Review
- Comparative pharmacokinetics of periplocin and its four key metabolites in rats after oral administration of periplocin and cardiac glycoside extract fromFrontiers in pharmacology · 2026Article
- RIP3 orchestrates oxidative stress and pyroptosis in doxorubicin-induced cardiotoxicity through regulation of AKT/Nrf2 signaling cascade.Molecular and cellular biochemistry · 2025Article
- Trillin protects against doxorubicin-induced cardiotoxicity through regulating Nrf2/HO-1 signaling pathway.PloS one · 2025Article
- NLRP3 inflammasome as a therapeutic target in doxorubicin-induced cardiotoxicity: role of phytochemicals.Frontiers in pharmacology · 2025Review
- Omega-3 supplementation attenuates doxorubicin-induced cardiotoxicity but is not related to the ceramide pathway.Food science & nutrition · 2024Article
- Using Omics to Identify Novel Therapeutic Targets in Heart Failure.Circulation. Genomic and precision medicine · 2024Review
- Ceramides: a potential cardiovascular biomarker in young adult childhood cancer survivors?European heart journal open · 2024Article
- The mCardiovascular diagnosis and therapy · 2024Article
- Nrf2: a dark horse in doxorubicin-induced cardiotoxicity.Cell death discovery · 2023Review
- Dual targets of lethal apoptosis and protective autophagy in liver cancer with periplocymarin elicit a limited therapeutic effect.International journal of oncology · 2023Article
- FUNDC1 protects against doxorubicin-induced cardiomyocyte PANoptosis through stabilizing mtDNA via interaction with TUFM.Cell death & disease · 2022Article
- Metabolomic Profiles on Antiblastic Cardiotoxicity: New Perspectives for Early Diagnosis and Cardioprotection.Journal of clinical medicine · 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-driven cardiotoxicity could result in dilated cardiomyopathy and heart failure (HF). Previously, we showed that periplocymarin exerted a cardiotonic role by promoting calcium influx and attenuating myocardial fibrosis induced by isoproterenol (ISO) by improving the metabolism of cardiomyocytes. However, the impact of periplocymarin on doxorubicin (DOX)-triggered cardiomyopathy has not been investigated. In the current study, C57BL/6 mice were randomly divided into three groups, namely, the control, DOX, and DOX+periplocymarin groups. The cardiac function and apoptosis were measured. Our results revealed that periplocymarin administration greatly improved the DOX-induced cardiac dysfunction manifested by the ejection fraction (EF%), fractional shortening (FS%), left ventricular posterior wall thickness (LVPW), left ventricular anterior wall thickness (LVAW), left ventricular (LV) mass, and attenuated DOX-induced cardiomyocyte apoptosis assessed by hematoxylin and eosin (H&E) staining, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining, and western blotting. Further study using H9c2 cells revealed that the pretreatment of periplocymarin suppressed DOX-induced apoptosis evidenced by annexin V staining. Moreover, liquid chromatography with tandem mass spectrometry (LC-MS/MS) analysis demonstrated that DOX lead to an accumulation in serum ceramide, and the pre-treatment of periplocymarin could reverse this phenomenon. Network pharmacology also demonstrated that ceramide metabolism was involved in the process. Consistently, real-time PCR showed that periplocymarin significantly abolished the induction of the genes involved in the
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