ArticleFrontiers in physiology2018
Proteomics Analysis of Myocardial Tissues in a Mouse Model of Coronary Microembolization.
Article in Frontiers in physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Molecular mechanisms of coronary microembolization-induced MINOCA.Basic research in cardiology · 2026Review
- Methodological Aspects of μLC-MS/MS for Wide-Scale Proteomic Analysis of Anthracycline-Induced Cardiomyopathy.ACS omega · 2025Article
- Enhanced Parkin-mediated mitophagy mitigates adverse left ventricular remodelling after myocardial infarction: role of PR-364.European heart journal · 2025Article
- Article
- Transcriptomic Analysis of Cardiac Tissues in a Rodent Model of Coronary Microembolization.Journal of inflammation research · 2024Article
- Association between NLRP3 inflammasome and periprocedural myocardial injury following elective PCI.Heliyon · 2023Article
- Applications of Tandem Mass Spectrometry (MS/MS) in Protein Analysis for Biomedical Research.Molecules (Basel, Switzerland) · 2022Review
- Sex-related differences of early cardiac functional and proteomic alterations in a rat model of myocardial ischemia.Journal of translational medicine · 2021Article
- TNF-α differentially modulates subunit levels of respiratory electron transport complexes of ER/PR +ve/-ve breast cancer cells to regulate mitochondrial complex activity and tumorigenic potential.Cancer & metabolism · 2021Article
- Cardiac Proteome Profiling in Ischemic and Dilated Cardiomyopathy Mouse Models.Frontiers in physiology · 2019Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Coronary microembolization (CME) is an important clinical problem, and it is related to poor outcome. The specific molecular mechanisms of CME are not fully understood. In the present study, we established a mice model of CME. Isobaric tags for relative and absolute quantitation (iTRAQ) and liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS) technologies identified 249 differentially expressed proteins in the myocardial tissues of CME mice as compared with sham-operated mice. Bioinformatics analysis demonstrated that these differentially expressed proteins were enriched in several energy metabolism or cytoskeleton organization related processes or pathways. Quantitative PCR and Western blotting validation experiments revealed that succinate dehydrogenase (SDHA and SDHB) were upregulated, Rho GDP dissociation inhibitor α (RhoGDIα) and Filamin-A (FLNA) were downregulated significantly in CME mice. These findings indicated that the alternations of the cytoskeleton and energy metabolism pathways play important roles in the pathogenesis of CME, future studies are warranted to verify if targeting these molecules might be useful to alleviate CME injury or not.
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Registered trials
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