ArticleBasic research in cardiology2025
Evolocumab attenuates myocardial ischemia/reperfusion injury by blocking PCSK9/LIAS-mediated cuproptosis of cardiomyocytes.
Article in Basic research in cardiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The trial behind it
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Who cites it
20 citing papers in PubMed.
- Cuproptosis and ferroptosis: signal pathways, diseases and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Iron, Copper, and Zinc Dyshomeostasis in Cardiovascular and Cerebrovascular Diseases: Redox Mechanisms, Evidence Levels, and Translational Prospects.International journal of molecular sciences · 2026Review
- PCSK9 alleviates doxorubicin‑induced pyroptosis of cardiomyocytes.Molecular medicine reports · 2026Article
- Advances in ferroptosis and cuproptosis: implications for spinal cord injury.Molecular biology reports · 2026Review
- METTL14 Promotes Cuproptosis-Associated Changes in Rats With Myocardial Ischemia-Reperfusion Injury.Journal of cellular biochemistry · 2026Article
- From copper transport to cuproptosis: emerging therapeutic targets in cardiovascular disease.Molecular and cellular biochemistry · 2026Review
- Post-translational modifications of mitochondrion-related proteins: integrative orchestrators of cell fate networks in cardiovascular disease.Cell communication and signaling : CCS · 2026Review
- Pyroptosis: Novel Targets in Molecular Mechanisms and Drug Therapy Research for Myocardial Ischemia Reperfusion Injury.Reviews in cardiovascular medicine · 2026Review
- Association Between PCSK9 Inhibitor Use and Risk of Age-Related Macular Degeneration.Translational vision science & technology · 2026Article
- Exploration of the Potential Mechanism of Metal Ion Transport-Related Genes in Myocardial Infarction Based on Transcriptomics.Journal of cellular and molecular medicine · 2026Article
- Cuproptosis: Biomarkers, Mechanisms and Treatments in Diseases.Molecules (Basel, Switzerland) · 2026Review
- LDL receptor-independent mechanisms of proprotein convertase subtilisin/kexin type 9 in cardiovascular pathophysiology.Frontiers in cardiovascular medicine · 2026Review
- Adipose-derived mesenchymal stem cell exosomes ameliorate copper metabolism dysregulation and reduce cuproptosis caused by liver IRI.Frontiers in veterinary science · 2026Article
- Pervasive environmental contaminant acrolein compromises myocardial geometry and function through the induction of cuproptosis.Acta biochimica et biophysica Sinica · 2025Article
- Functional nano-nucleic acid platform promotes copper-induced gastric cancer cell death.RSC advances · 2025Article
- Proprotein Convertase Subtilisin/Kexin Type 9 (PCSK9): The Multifaceted Biology, Diseases, and Pharmaceutical Interventions.MedComm · 2025Review
- Cuproptosis and Cardiovascular Diseases: Mechanisms, Pathophysiology, and Therapeutic Strategies-A Narrative Review.Reviews in cardiovascular medicine · 2025Review
- The Impact of PCSK9 on Diabetic Cardiomyopathy: Mechanisms and Implications.Biomolecules · 2025Review
- Cuproptosis: a novel therapeutic mechanism in lung cancer.Cancer cell international · 2025Review
- PCSK9 Manipulates Lipid Metabolism and the Immune Microenvironment in Cancer.OncoTargets and therapy · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Myocardial ischemia‒reperfusion (I/R) injury is the crucial cause of poor prognosis after revascularization in patients with myocardial infarction (MI) due to the lack of specific therapeutic drugs. Proprotein convertase subtilisin/Kexin type 9 (PCSK9) is related to the pathogenesis and progression of various cardiovascular diseases. However, the specific role of PCSK9 in I/R-induced cardiac injury remains to be further investigated. In this study, wild-type (WT) C57BL/6J mice were administered evolocumab (a monoclonal antibody of PCSK9) before I/R surgery. Cardiac damage and function were assessed by echocardiography and TTC/Evans Blue staining. Inflammation, oxidative stress, mitochondrial dysfunction, and cuproptosis were evaluated by histopathology and qPCR. The interaction between proteins was confirmed by protein docking and co-immunoprecipitation. Our data revealed that PCSK9 level was increased in I/R-induced mouse serum and hearts and in serum of MI patients. Furthermore, evolocumab significantly improved cardiac injury and dysfunction, inflammation, oxidative stress, and cuproptosis. Mechanistically, evolocumab obstructs the direct interaction of PCSK9 and LIAS, and subsequently inhibits cardiomyocyte cuproptosis. In conclusion, inhibition of PCSK9 alleviates I/R-induced cardiac remodeling and dysfunction by targeting LIAS-mediated cuproptosis, which may be a novel therapeutic strategy for patients with ischemic cardiomyopathy.
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Registered trials
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