ArticleJournal of immunology (Baltimore, Md. : 1950)2018
Contribution of Adipose-Derived Factor D/Adipsin to Complement Alternative Pathway Activation: Lessons from Lipodystrophy.
Article in Journal of immunology (Baltimore, Md. : 1950), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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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Who cites it
53 citing papers in PubMed, 79 citations in OpenAlex.
- Peritoneal ovarian cancer growth in the omentum proceeds independently of mature adipocytes.Nature communications · 2026Article
- Diagnostic performance of urinary adipsin as a screening biomarker for pre-eclampsia.International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics · 2026Article
- Treatment of atypical hemolytic uremic syndrome and C3 glomerulopathy in mice by hepatic expression of factor D.Blood advances · 2026Article
- Advances in Adipose Tissue Biology.Endocrine reviews · 2026Review
- Activation of the alternative complement pathway and its relevance for sodium retention in experimental nephrotic syndrome.Pflugers Archiv : European journal of physiology · 2026Article
- Complement factor D (adipsin) mediates pressure-pain hypersensitivity post destabilization of medial meniscus injury.Arthritis research & therapy · 2025Article
- Adipocytes are dispensable in shaping the ovarian cancer tumor microenvironment in the omentum.bioRxiv : the preprint server for biology · 2025Article
- Friend or foe: assessing the value of animal models for facilitating clinical breakthroughs in complement research.The Journal of clinical investigation · 2025Review
- Regulation of the terminal complement cascade in adipose tissue for control of its volume, cellularity, and fibrosis.Obesity (Silver Spring, Md.) · 2025Review
- Adipose-derived leptin and complement factor D mediate osteoarthritis severity and pain.Science advances · 2025Article
- Improved therapeutic efficacy of a bifunctional anti-C5 mAb-FH SCR1-5 fusion protein over anti-C5 mAb in an accelerated mouse model of C3 glomerulopathy.ImmunoHorizons · 2025Article
- Factor B as a therapeutic target for the treatment of complement-mediated diseases.Frontiers in immunology · 2025Review
- Role of Complement in Liver Diseases.Seminars in liver disease · 2024Review
- Is the endotoxin-complement cascade the major driver in lipedema?Trends in endocrinology and metabolism: TEM · 2024Review
- Article
- Adipsin in the pathogenesis of cardiovascular diseases.Vascular pharmacology · 2024Review
- C3 Glomerulopathy: Novel Treatment Paradigms.Kidney international reports · 2024Review
- C3G and Ig-MPGN-treatment standard.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2024Review
- The Relationship between Complements and Age-Related Macular Degeneration and Its Pathogenesis.Journal of ophthalmology · 2024Review
- Complement inhibitors for age-related macular degeneration.The Cochrane database of systematic reviews · 2023Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Factor D (FD) is an essential component of the complement alternative pathway (AP). It is an attractive pharmaceutical target because it is an AP-specific protease circulating in blood. Most components of the complement activation pathways are produced by the liver, but FD is highly expressed by adipose tissue. Two critical questions are: 1) to what degree does adipose tissue contribute to circulating FD levels and 2) what quantity of FD is sufficient to maintain a functional AP? To address these issues, we studied a novel mouse strain with complete lipodystrophy (LD), the fld mouse with partial LD, an FD-deficient mouse, and samples from lipodystrophic patients. FD was undetectable in the serum of LD mice, which also showed minimal AP function. Reconstitution with purified FD, serum mixing experiments, and studies of partial LD mice all demonstrated that a low level of serum FD is sufficient for normal AP activity in the mouse system. This conclusion was further supported by experiments in which wild-type adipose precursors were transplanted into LD mice. Our results indicate that almost all FD in mouse serum is derived from adipose tissue. In contrast, FD levels were reduced ∼50% in the sera of patients with congenital generalized LD. Our studies further demonstrate that a relatively small amount of serum FD is sufficient to facilitate significant time-dependent AP activity in humans and in mice. Furthermore, this observation highlights the potential importance of obtaining nearly complete inhibition of FD in treating alternative complement activation in various autoimmune and inflammatory human 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.