ArticleNature communications2019
Serum FHR1 binding to necrotic-type cells activates monocytic inflammasome and marks necrotic sites in vasculopathies.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 66 citations in OpenAlex.
- Screening for candidate genes and cell populations associated with atherosclerotic calcification using single-cell RNA sequencing.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
- Association of FHR5 With Disease Severity in ANCA-Associated Vasculitis.Kidney international reports · 2026Article
- Extended haplotypes at the complement factor H gene locus are associated with liver transplant rejection.Hepatology communications · 2026Article
- Malondialdehyde epitopes exposed on dying cells are potent modulators of complement activity and efferocytosis.Journal of lipid research · 2026Article
- Satellite microglia-like cells in human dorsal root ganglia and changes with diabetic neuropathy.bioRxiv : the preprint server for biology · 2026Article
- Adhesion G protein-coupled receptors.Pharmacological reviews · 2026Review
- Therapeutic targeting of adhesion GPCRs: a status update and future potential.Expert opinion on drug discovery · 2026Review
- Complement-Mediated Kidney Diseases: Role of Alternative Pathway in Glomerular Inflammation.Kidney international reports · 2026Review
- Deletion of the Mouse Homolog of Human FHR1 (muFHR1) Alleviates Atherosclerosis in ApoE-/- mice.International journal of medical sciences · 2026Article
- Dual Role of Factor H-Related Protein 1 in IgA Nephropathy Kidney Injury.Kidney international reports · 2026Article
- A new perspective on AMD pathogenesis: a sequential Factor H-centered view of complement dysregulation.Frontiers in immunology · 2026Review
- Polyporusterone B Alleviates Inflammatory Injury via Suppression of Pro-Inflammatory Cytokine Production.International journal of molecular sciences · 2025Article
- Factor-H-related protein 1 (FHR1), a promotor of para-inflammation in age-related macular degeneration.Journal of neuroinflammation · 2025Article
- Mechanosensitive adhesion G protein-coupled receptors: Insights from health and disease.Genes & diseases · 2025Review
- Factor H-related 2 levels dictate FHR dimer composition.Scientific reports · 2025Article
- Associations between plasma metabolism-associated proteins and future development of giant cell arteritis: results from a prospective study.Rheumatology (Oxford, England) · 2025Article
- Long-lasting changes in circulating dendritic cell and monocyte subsets, and altered expression of EMR2, CD97 and EMR3 on these cells in the posttraumatic course.Clinical & translational immunology · 2025Article
- The Complement System.Advances in experimental medicine and biology · 2025Review
- Factor H-related 1 and heparan sulfate architecture contribute to complement dysregulation in C3 glomerulopathy.Frontiers in immunology · 2025Article
- Aberrant Lipid Metabolism and Complement Activation in Age-Related Macular Degeneration.Investigative ophthalmology & visual science · 2024Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
Persistent inflammation is a hallmark of many human diseases, including anti-neutrophil cytoplasmic antibody-associated vasculitis (AAV) and atherosclerosis. Here, we describe a dominant trigger of inflammation: human serum factor H-related protein FHR1. In vitro, this protein selectively binds to necrotic cells via its N-terminus; in addition, it binds near necrotic glomerular sites of AAV patients and necrotic areas in atherosclerotic plaques. FHR1, but not factor H, FHR2 or FHR3 strongly induces inflammasome NLRP3 in blood-derived human monocytes, which subsequently secrete IL-1β, TNFα, IL-18 and IL-6. FHR1 triggers the phospholipase C-pathway via the G-protein coupled receptor EMR2 independent of complement. Moreover, FHR1 concentrations of AAV patients negatively correlate with glomerular filtration rates and associate with the levels of inflammation and progressive disease. These data highlight an unexpected role for FHR1 during sterile inflammation, may explain why FHR1-deficiency protects against certain diseases, and identifies potential targets for treatment of auto-inflammatory diseases.
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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.