ArticleAmerican journal of translational research2017
Qiliqiangxin attenuates isoproterenol-induced cardiac remodeling in mice.
Article in American journal of translational research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Imbalance of the Regulated Cell Death and Autophagic Network: A Core Mechanism Driving Toxicological and Ischemic Myocardial Injury and a Target for Intervention with Traditional Chinese Medicine.Cardiovascular toxicology · 2026Review
- Isoproterenol mechanisms in inducing myocardial fibrosis and its application as an experimental model for the evaluation of therapeutic potential of phytochemicals and pharmaceuticals.Animal models and experimental medicine · 2025Review
- Research on the mechanism of the anti-myocardial infarction effect of the Qiliqiangxin capsule on heart failure rats via nontargeted metabolomics and lipidomics.BMC cardiovascular disorders · 2024Article
- Review
- Study protocol: Traditional Chinese Medicine (TCM) syndrome differentiation for heart failure patients and its implication for long-term therapeutic outcomes of the Qiliqiangxin capsules.Chinese medicine · 2021Article
- Traditional Chinese Medication Qiliqiangxin Attenuates Diabetic Cardiomyopathy via Activating PPARγ.Frontiers in cardiovascular medicine · 2021Article
- Nobiletin Attenuates Pathological Cardiac Remodeling after Myocardial Infarction via Activating PPARPPAR research · 2021Article
- Article
- Study protocol for a randomized controlled trial: Qiliqiangxin in heart failUre: assESsment of reduction in morTality (QUEST).BMC complementary medicine and therapies · 2020Article
- CD47 antibody suppresses isoproterenol-induced cardiac hypertrophy through activation of autophagy.American journal of translational research · 2020Article
- Qiliqiangxin attenuates atrial structural remodeling in prolonged pacing-induced atrial fibrillation in rabbits.Naunyn-Schmiedeberg's archives of pharmacology · 2019Article
- Exercise Mediated Nrf2 Signaling Protects the Myocardium From Isoproterenol-Induced Pathological Remodeling.Frontiers in cardiovascular medicine · 2019Article
- CD47 Deficiency Attenuates Isoproterenol-Induced Cardiac Remodeling in Mice.Oxidative medicine and cellular longevity · 2019Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTo further explore the role of PPARγ in QL treatment, ISO-induced mice model and following methods were established.
methodsCardiac remodeling on mice model was induced by isoproterenol (ISO) infusion or saline infusion as control for two weeks then divided into 4 groups, after that divided in 5 different treatment methods to investigate the role of PPARγ in QL therapy. Echocardiography and Masson's trichrome staining were respectively used to determine cardiac function and fibrosis. Immunoblotting was applied to evaluate the expression levels of proliferator-activated receptor-γ (PPARγ), Bax, Bcl, phospho-Akt (Ser473), Akt, phospho-P38 and P38, phosphor-ERK and ERK.
resultsQL treatment improved left ventricular function, decreased apoptosis, and prevented myocardial fibrosis at the same time. Meanwhile, the PPARγ level was elevated with QL treatment in ISO-injected mice hearts. Inhibition of PPARγ activity blocked the protective effects of QL, while the activator of PPARγ did not provide additional benefit. Specifically, the results indicated a decline in PPARγ in ISO-infused mice and QL decreased the toxicity of ISO by improving the level of PPARγ.
conclusionsOur study demonstrated that QL treatment provided cardioprotection against ISO-induced cardiac remodeling by improving PPARγ level, which could be as the potential therapeutic target in reversing cardiac remodeling and heart failure.
Indexed as
Identifiers
29312510PMC5752908W2942696240What OpenQuestion holds
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.