ArticleJournal of inflammation research2021
Monomeric CRP Aggravates Myocardial Injury After Myocardial Infarction by Polarizing the Macrophage to Pro-Inflammatory Phenotype Through JNK Signaling Pathway.
Article in Journal of inflammation research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
- The Efficacy and Safety of Bisoprolol in the Treatment of Myocardial Infarction with Cardiac Insufficiency.Computational and mathematical methods in medicine · 2022Trial
- C-Reactive Protein-Triglyceride Glucose Index and Mortality in Patients with Ventricular Septal Rupture After Acute Myocardial Infarction.Journal of inflammation research · 2026Article
- The CALLY index as a novel predictor of left ventricular aneurysm in patients with ST-segment elevation myocardial infarction.Frontiers in cardiovascular medicine · 2026Article
- Brain heart crosstalk after ischemic stroke toward a unified framework for pathophysiology and precision medicine.Frontiers in molecular neuroscience · 2026Review
- Monomeric C-reactive Protein Exacerbates Neuronal Injury and Enhances Microglial Activation after Global Cerebral Ischemia in Mice.Molecular neurobiology · 2025Article
- An aptamer specifically targeting mCRP ameliorates experimental arthritis.Journal of orthopaedic translation · 2025Article
- The Pathogenic Role of C-Reactive Protein in Diabetes-Linked Unstable Atherosclerosis.International journal of molecular sciences · 2025Review
- Immunometabolic Interactions in Obesity: Implications for Therapeutic Strategies.Biomedicines · 2025Review
- A conformational change of C-reactive protein drives neutrophil extracellular trap formation in inflammation.BMC biology · 2025Article
- Mechanism and research progress of MAPK signaling pathway in myocardial fibrosis.Frontiers in cardiovascular medicine · 2025Review
- C-reactive protein: the nexus between inflammation and protein misfolding diseases.Frontiers in immunology · 2025Review
- Redefining CRP in tissue injury and repair: more than an acute pro-inflammatory mediator.Frontiers in immunology · 2025Review
- Macrophages in organ fibrosis: from pathogenesis to therapeutic targets.Cell death discovery · 2024Review
- Review
- The interplay between T lymphocytes and macrophages in myocardial ischemia/reperfusion injury.Molecular and cellular biochemistry · 2024Review
- mCRP-Induced Focal Adhesion Kinase-Dependent Monocyte Aggregation and M1 Polarization, Which Was Partially Blocked by the C10M Inhibitor.International journal of molecular sciences · 2024Article
- Role of macrophage polarization in heart failure and traditional Chinese medicine treatment.Frontiers in pharmacology · 2024Review
- Higher monomeric C-reactive protein levels are associated with premature coronary artery disease.Frontiers in immunology · 2024Article
- C-Reactive Protein in Atherosclerosis-More than a Biomarker, but not Just a Culprit.Reviews in cardiovascular medicine · 2023Review
- C-Reactive Protein: Pathophysiology, Diagnosis, False Test Results and a Novel Diagnostic Algorithm for Clinicians.Diseases (Basel, Switzerland) · 2023Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveA polarized macrophage response plays a critical role in the pathophysiological process of myocardial infarction (MI). Several studies have shown a pro-inflammatory role for monomeric C-reactive protein (mCRP) in cardiovascular disease. However, the mechanism of how mCRP regulates macrophage phenotype switching remains unknown. In the present study, the effect of mCRP on macrophage polarization and its pathological function in myocardial repair after myocardial infarction was investigated.
methodsMI was induced by permanent ligation of the left anterior descending coronary artery in ICR mice. Adult mice were injected with mCRP (2.5 mg/kg) with or without SP600125 (15 mg/kg, JNK inhibitor) 45 min before MI. The cardiac function, scar size as well as cardiac fibrosis, infiltration of inflammatory cells, and the level of proteins in the JNK signaling pathway in infarcted myocardium were assessed. In addition, the phenotypic characterization of macrophages was further measured by ELISA, flow cytometry and quantitative RT-PCR in cultured THP-1 cells or peritoneal macrophages.
resultsCardiac function deterioration, ventricular dilatation and fibrosis were exacerbated in mice pretreatment with mCRP following MI. Meanwhile, an increased accumulation of infiltrated inflammatory cells in infarcted myocardium was observed in the mCRP group. Moreover, activation of the JNK signaling pathway was markedly elevated in mCRP treated animals post-MI. In contrast, pharmacological inhibition of JNK phosphorylation activity by SP600125 muted the detrimental effects of mCRP in MI mice. Furthermore, in vitro and in vivo co-culture experiments showed that mCRP shifted macrophage polarization towards pro-inflammatory phenotypes, and this polarization could be abolished by sp600125.
conclusionTaken together, our results imply that mCRP impairs myocardial repair after myocardial infarction by polarizing the macrophages into the pro-inflammatory M1 phenotype via the JNK-dependent pathway.
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