ReviewMediators of inflammation2014
Recognition functions of pentameric C-reactive protein in cardiovascular disease.
Review in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
26 citing papers in PubMed, 93 citations in OpenAlex.
- C-reactive protein in cardiovascular disease: clinical associations, conformation-dependent biology, and therapeutic perspectives.Frontiers in immunology · 2026Review
- Cardiac Involvement in Eosinophilic Granulomatosis with Polyangiitis.Current cardiology reports · 2025Review
- C-reactive protein: the nexus between inflammation and protein misfolding diseases.Frontiers in immunology · 2025Review
- An evolutionarily conserved function of C-reactive protein is to prevent the formation of amyloid fibrils.Frontiers in immunology · 2024Article
- C-Reactive Protein: Pathophysiology, Diagnosis, False Test Results and a Novel Diagnostic Algorithm for Clinicians.Diseases (Basel, Switzerland) · 2023Review
- Structurally Altered, Not Wild-Type, Pentameric C-Reactive Protein Inhibits Formation of Amyloid-β Fibrils.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- LncRNA TTTY15 knockdown alleviates HMolecular and cellular biochemistry · 2021Article
- Pattern Recognition Proteins: First Line of Defense Against Coronaviruses.Frontiers in immunology · 2021Review
- Therapeutic Lowering of C-Reactive Protein.Frontiers in immunology · 2020Review
- Complement Activation by C-Reactive Protein Is Critical for Protection of Mice Against Pneumococcal Infection.Frontiers in immunology · 2020Article
- Treatment of Pneumococcal Infection by Using Engineered Human C-Reactive Protein in a Mouse Model.Frontiers in immunology · 2020Article
- Conformationally Altered C-Reactive Protein Capable of Binding to Atherogenic Lipoproteins Reduces Atherosclerosis.Frontiers in immunology · 2020Article
- The Multiple Faces of C-Reactive Protein-Physiological and Pathophysiological Implications in Cardiovascular Disease.Molecules (Basel, Switzerland) · 2019Review
- Hyper-acidic fusion minipeptides escort the intrinsic antioxidative ability of the pattern recognition receptor CRP in non-animal organisms.Scientific reports · 2019Article
- Functionality of C-Reactive Protein for Atheroprotection.Frontiers in immunology · 2019Review
- Structure-Function Relationships of C-Reactive Protein in Bacterial Infection.Frontiers in immunology · 2019Review
- Evolution of C-Reactive Protein.Frontiers in immunology · 2019Review
- Combined Use of Neutrophil to Lymphocyte Ratio and C-Reactive Protein Level to Predict Clinical Outcomes in Acute Myocardial Infarction Patients Undergoing Percutaneous Coronary Intervention.Korean circulation journal · 2017Article
- Functional Transformation of C-reactive Protein by Hydrogen Peroxide.The Journal of biological chemistry · 2017Article
- Transitional changes in the CRP structure lead to the exposure of proinflammatory binding sites.Nature communications · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
C-reactive protein (CRP) performs two recognition functions that are relevant to cardiovascular disease. First, in its native pentameric conformation, CRP recognizes molecules and cells with exposed phosphocholine (PCh) groups, such as microbial pathogens and damaged cells. PCh-containing ligand-bound CRP activates the complement system to destroy the ligand. Thus, the PCh-binding function of CRP is defensive if it occurs on foreign pathogens because it results in the killing of the pathogen via complement activation. On the other hand, the PCh-binding function of CRP is detrimental if it occurs on injured host cells because it causes more damage to the tissue via complement activation; this is how CRP worsens acute myocardial infarction and ischemia/reperfusion injury. Second, in its nonnative pentameric conformation, CRP also recognizes atherogenic low-density lipoprotein (LDL). Recent data suggest that the LDL-binding function of CRP is beneficial because it prevents formation of macrophage foam cells, attenuates inflammatory effects of LDL, inhibits LDL oxidation, and reduces proatherogenic effects of macrophages, raising the possibility that nonnative CRP may show atheroprotective effects in experimental animals. In conclusion, temporarily inhibiting the PCh-binding function of CRP along with facilitating localized presence of nonnative pentameric CRP could be a promising approach to treat atherosclerosis and myocardial infarction. There is no need to stop the biosynthesis of CRP.
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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.