ReviewNature reviews. Cardiology2024
Canonical and non-canonical roles of complement in atherosclerosis.
Review in Nature reviews. Cardiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pharmacological and Genetic Targeting of Inflammatory Chemokine Receptors CCR1, CCR2, and CCR5 in Atherosclerosis: A Systematic Review and Meta-Analysis of Preclinical Studies.Journal of the American Heart Association · 2026Pooled it
- Article
- Complement Inhibition in the Clinic: Are We Doing Enough to Protect Patients From Infection?European journal of immunology · 2026Review
- Adventitial Niches, Complement and Inflammation in Pulmonary Vascular Disease: Current Status and Future Directions.Comprehensive Physiology · 2026Review
- Complement C3 recognition by C3 convertases.Science advances · 2026Article
- Immunoregulatory genebioRxiv : the preprint server for biology · 2026Article
- Cumulative average remnant cholesterol inflammatory index and risk of cardiometabolic multimorbidity: evidence from a prospective nationwide cohort study in China.Lipids in health and disease · 2026Article
- Complement Components C1r and C8 Serve as Potential Inflammatory Biomarkers for Coronary Heart Disease Severity: The Mediating Role of C-Reactive Protein.Journal of inflammation research · 2026Article
- B cells and B-cell receptor repertoire features in coronary heart disease: immunopathogenic roles, clinical relevance, and therapeutic potential.Frontiers in cardiovascular medicine · 2026Review
- Integrated multi-omics analysis reveals gut microbiota and metabolic characteristics in coronary heart disease.Frontiers in microbiology · 2026Article
- Integrative Multi-Omics and Machine Learning Reveal Shared Biomarkers in Type 2 Diabetes and Atherosclerosis.International journal of molecular sciences · 2025Article
- The complement cascade in Alzheimer's disease: modern implications of an ancient immune protagonist.Molecular neurodegeneration · 2025Review
- A single-cell atlas reveals the tumorigenesis and microenvironment status of primary tracheobronchial tumors.NPJ precision oncology · 2025Article
- Article
- Proteolytic profiling of human plasma reveals an immunoactive complement C3 fragment.The EMBO journal · 2025Article
- Metabolic Vulnerability Index and Atherosclerosis Incident: A Prospective Cohort Study From the UK Biobank.Journal of the American Heart Association · 2025Article
- Complement C3 in panvascular disease: a central integrator of immune signaling and vascular remodeling.Clinical science (London, England : 1979) · 2025Review
- The Multifaceted Role of Platelets in Atherosclerosis and Ischemic Disease: Pathogenesis, Inflammation, and Therapeutic Opportunities.Life (Basel, Switzerland) · 2025Review
- Review
- Potentially Atherogenic Combined Biochemical and Physiological Changes in Human Antiorthostatic Hypokinesia.Bulletin of experimental biology and medicine · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Cardiovascular diseases are the leading cause of death globally, and atherosclerosis is the major contributor to the development and progression of cardiovascular diseases. Immune responses have a central role in the pathogenesis of atherosclerosis, with the complement system being an acknowledged contributor. Chronic activation of liver-derived and serum-circulating canonical complement sustains endothelial inflammation and innate immune cell activation, and deposition of complement activation fragments on inflamed endothelial cells is a hallmark of atherosclerotic plaques. However, increasing evidence indicates that liver-independent, cell-autonomous and non-canonical complement activities are underappreciated contributors to atherosclerosis. Furthermore, complement activation can also have atheroprotective properties. These specific detrimental or beneficial contributions of the complement system to the pathogenesis of atherosclerosis are dictated by the location of complement activation and engagement of its canonical versus non-canonical functions in a temporal fashion during atherosclerosis progression. In this Review, we summarize the classical and the emerging non-classical roles of the complement system in the pathogenesis of atherosclerosis and discuss potential strategies for therapeutic modulation of complement for the prevention and treatment of atherosclerotic cardiovascular disease.
Indexed as
Identifiers
38600367What OpenQuestion holds
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.