ArticleAmerican journal of physiology. Renal physiology2017
Pericytes and immune cells contribute to complement activation in tubulointerstitial fibrosis.
Article in American journal of physiology. Renal physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.
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Who cites it
52 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.
- C1q as a target molecule to treat human disease: What do mouse studies teach us?Frontiers in immunology · 2022Pooled it
- The E3 ubiquitin ligase Itch plays an essential role in kidney fibrosis by inhibiting Dvl2/GSK3β/β-catenin signaling pathway.Cell death and differentiation · 2026Article
- Complement activation in anti-glomerular basement membrane disease before and after treatment with imlifidase.Clinical kidney journal · 2026Article
- The temporal gene expression landscape of rhabdomyolysis-induced acute kidney injury reveals the timing of complement activation.Communications biology · 2025Article
- Nicotinamide Attenuates Complement and Coagulation Pathways and Resultant Renal Fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- The Pathogenesis, Potential Biomarkers and Novel Therapeutic Strategies for Tubulointerstitial Nephritis in Systemic Lupus Erythematosus-A Narrative Review.International journal of molecular sciences · 2025Review
- Role of local complement activation in kidney fibrosis and repair.The Journal of clinical investigation · 2025Review
- Article
- Chronic kidney disease enhances alternative pathway activity: a new paradigm.The Journal of clinical investigation · 2025Review
- Complement factors as biomarkers in ANCA-associated vasculitis in remission.Clinical and experimental immunology · 2025Article
- Renal Epithelial Complement C3 Expression Affects Kidney Fibrosis Progression.International journal of molecular sciences · 2024Article
- Urinary Biomarkers for Lupus Nephritis: A Systems Biology Approach.Journal of clinical medicine · 2024Review
- Decoding spatiotemporal transcriptional dynamics and epithelial fibroblast crosstalk during gastroesophageal junction development through single cell analysis.Nature communications · 2024Article
- From Acute to Chronic: Unraveling the Pathophysiological Mechanisms of the Progression from Acute Kidney Injury to Acute Kidney Disease to Chronic Kidney Disease.International journal of molecular sciences · 2024Review
- Complement Cascade Proteins Correlate with Fibrosis and Inflammation in Early-Stage Type 1 Diabetic Kidney Disease in the Ins2Akita Mouse Model.International journal of molecular sciences · 2024Article
- Urinary complement biomarkers in immune-mediated kidney diseases.Frontiers in immunology · 2024Review
- Analysis of complement system and its related factors in Alzheimer's disease.BMC neurology · 2023Article
- Urine Proteomics Link Complement Activation with Interstitial Fibrosis/Tubular Atrophy in Lupus Nephritis Patients.Seminars in arthritis and rheumatism · 2023Article
- Role of perivascular cells in kidney homeostasis, inflammation, repair and fibrosis.Nature reviews. Nephrology · 2023Review
- IgA nephropathy associated with Crohn's disease.World journal of methodology · 2023Review
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 1 country.
Funding
Abstract
We have examined the pathogenic role of increased complement expression and activation during kidney fibrosis. Here, we show that PDGFRβ-positive pericytes isolated from mice subjected to obstructive or folic acid injury secrete C1q. This was associated with increased production of proinflammatory cytokines, extracellular matrix components, collagens, and increased Wnt3a-mediated activation of Wnt/β-catenin signaling, which are hallmarks of myofibroblast activation. Real-time PCR, immunoblots, immunohistochemistry, and flow cytometry analysis performed in whole kidney tissue confirmed increased expression of C1q, C1r, and C1s as well as complement activation, which is measured as increased synthesis of C3 fragments predominantly in the interstitial compartment. Flow studies localized increased C1q expression to PDGFRβ-positive pericytes as well as to CD45-positive cells. Although deletion of C1qA did not prevent kidney fibrosis, global deletion of C3 reduced macrophage infiltration, reduced synthesis of C3 fragments, and reduced fibrosis. Clodronate mediated depletion of CD11bF4/80 high macrophages in UUO mice also reduced complement gene expression and reduced fibrosis. Our studies demonstrate local synthesis of complement by both PDGFRβ-positive pericytes and CD45-positive cells in kidney fibrosis. Inhibition of complement activation represents a novel therapeutic target to ameliorate fibrosis and progression of chronic kidney disease.
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Registered trials
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