ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2020
Emerging protective roles of shengmai injection in septic cardiomyopathy in mice by inducing myocardial mitochondrial autophagy via caspase-3/Beclin-1 axis.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- Immunometabolic chaos in septic shock.Journal of leukocyte biology · 2025Article
- Neferine inhibits BMECs pyroptosis and maintains blood-brain barrier integrity in ischemic stroke by triggering a cascade reaction of PGC-1α.Scientific reports · 2024Article
- Therapeutic Strategies Targeting Mitochondrial Dysfunction in Sepsis-induced Cardiomyopathy.Cardiovascular drugs and therapy · 2024Review
- Review of the Predictive Value of Biomarkers in Sepsis Mortality.Emergency medicine international · 2024Review
- Traditional Chinese medicine for treatment of sepsis and related multi-organ injury.Frontiers in pharmacology · 2023Review
- Article
- Protective Effect of Natural Medicinal Plants on Cardiomyocyte Injury in Heart Failure: Targeting the Dysregulation of Mitochondrial Homeostasis and Mitophagy.Oxidative medicine and cellular longevity · 2022Review
- Analysis of the role and mechanism of EGCG in septic cardiomyopathy based on network pharmacology.PeerJ · 2022Article
- Mitochondria-endoplasmic reticulum contacts in sepsis-induced myocardial dysfunction.Frontiers in cell and developmental biology · 2022Review
- Research Progress in Chinese Herbal Medicines for Treatment of Sepsis: Pharmacological Action, Phytochemistry, and Pharmacokinetics.International journal of molecular sciences · 2021Review
- Xuanfei Pingchuan Capsules Ameliorate Autophagy in Human Bronchial Epithelial Cells by Inhibiting p38 Phosphorylation.Frontiers in pharmacology · 2021Article
- A Quantitative Serum Proteomic Analysis Helps to Explore the Comprehensive Mechanism and Identify Serum Biomarkers of Shengmai Injection's Effect on Isoproterenol-Induced Myocardial Ischemia in Rats.Frontiers in pharmacology · 2021Article
- [Effect of small interfering RNA-mediated BIRC6 silencing on apoptosis and autophagy of renal cancer 786-O cells].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020Article
- SirT3 activates AMPK-related mitochondrial biogenesis and ameliorates sepsis-induced myocardial injury.Aging · 2020Article
Corrections and comments
- Retraction · 2023-02-16Duplication of/in Image · Investigation by Journal/Publisher · Investigation by Third Party · Paper Mill · Unreliable Data ·
- Retracted
Authors and funding
18 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundSepsis, a life-threatening systemic syndrome related to inflammatory response, usually accompanied by major organ dysfunctions. The aim of the present study was to elucidate the role by which Shengmai injection (SMI) acts to septic cardiomyopathy.
methodsInitially, the induced mice with septic cardiomyopathy were treated with SMI or normal saline (NS) with oe-caspase-3, and HL-1 cells were treated with oe-Beclin-1 and oe-caspase-3 and then cultured with lipopolysaccharide (LPS). Subsequently, we measured the cardiac troponin I (cTnI) level, and expression of mitochondrial autophagy protein (parkin and pink1) and myocardial cell autophagy-related proteins (LC3-II and LC3-I). Additionally, we identified the cleavage of Beclin-1 by caspase-3 and detected the changes of mitochondrial membrane potential, level of reactive oxygen species (ROS), and apoptosis of myocardial cells in myocardial tissues of mice.
resultsIt has been demonstrated that SMI contributed to the increase of myocardial mitochondrial autophagy, reduction of cTnI level, and elevation of mitochondrial membrane potential in septic cardiomyopathy mice. Both in vitro and in vivo experiments showed that caspase-3 promoted cleavage of Beclin-1 and release of ROS, whereas repressed lipopolysaccharide (LPS)-induced mitochondrial autophagy. Furthermore, the facilitation of myocardial mitochondrial autophagy and protection of myocardial mitochondria by SMI through inhibition of cleavage Beclin-1 by caspase-3 in septic cardiomyopathy mice were also proved by in vivo experiments.
conclusionTaken together, SMI could protect myocardial mitochondria by promoting myocardial mitochondrial autophagy in septic cardiomyopathy via inhibition of cleavage of Beclin-1 by caspase-3. Our study demonstrates that SMI could represent a novel target for treatment of septic cardiomyopathy.
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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.