ReviewImmunobiology2012
Complement-mediated injury and protection of endothelium: lessons from atypical haemolytic uraemic syndrome.
Review in Immunobiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
What it found
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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.
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
50 citing papers in PubMed, 92 citations in OpenAlex.
- Thrombotic microangiopathy in untreated myeloma patients receiving carfilzomib, cyclophosphamide and dexamethasone on the CARDAMON study.British journal of haematology · 2021Trial
- IPNA clinical practice recommendations for the management of aHUS and secondary TMA in children.Pediatric nephrology (Berlin, Germany) · 2026Article
- GWAS Meta-analysis Identifies Novel Associated Loci and Points to Causal Tissues in Central Serous Chorioretinopathy.medRxiv : the preprint server for health sciences · 2026Article
- Cellular Mechanisms Underlying Endothelial and Histopathological Alterations Induced by Cerebral Angiography.Journal of clinical medicine · 2026Review
- Modeling antithymocyte globulin-induced microvasculopathy using human iPSC-derived vascularized liver organoids.Cell reports. Medicine · 2025Article
- Activated Complement System's Impact in Antiphospholipid Syndrome Thrombosis: From Pathophysiology to Treatment.Journal of clinical medicine · 2025Review
- Current Understanding of the Pathogenesis of ANCA-Associated Vasculitis and Novel Treatment Options Targeting Complement Activation.Life (Basel, Switzerland) · 2025Review
- Advances in Research on the Release of von Willebrand Factor from Endothelial Cells through the Membrane Attack Complex C5b-9 in Sepsis.Journal of inflammation research · 2025Review
- Article
- Impact of smoking on the complement system: a narrative review.Frontiers in immunology · 2025Review
- Article
- Article
- More than a key-the pathological roles of SARS-CoV-2 spike protein in COVID-19 related cardiac injury.Sports medicine and health science · 2023Review
- Novel Classification of Thrombotic Disorders Based on Molecular Hemostasis and Thrombogenesis Producing Primary and Secondary Phenotypes of Thrombosis.Biomedicines · 2022Review
- Primary non-function in a deceased donor kidney transplant even with a Kidney Donor Risk Index less than 1.0: a case report.Korean journal of transplantation · 2022Article
- Molecular Pathogenesis of Endotheliopathy and Endotheliopathic Syndromes, Leading to Inflammation and Microthrombosis, and Various Hemostatic Clinical Phenotypes Based on "Two-Activation Theory of the Endothelium" and "Two-Path Unifying Theory" of Hemostasis.Medicina (Kaunas, Lithuania) · 2022Review
- Is the Endothelium the Missing Link in the Pathophysiology and Treatment of COVID-19 Complications?Cardiovascular drugs and therapy · 2022Review
- Targeting vascular inflammation through emerging methods and drug carriers.Advanced drug delivery reviews · 2022Review
- Mechanisms of vascular damage in ANCA vasculitis.Seminars in immunopathology · 2022Review
- Renal Endothelial Cytotoxicity Assay to Diagnose and Monitor Renal Transplant Recipients for Anti-Endothelial Antibodies.Frontiers in immunology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The complement system provides a vital defence against invading pathogens. As an intrinsic system it is always 'on', in a state of constant, low level activation. This activation is principally mediated through the deposition of C3b on to pathogenic surfaces and host tissues. C3b is generated by spontaneous 'tick over' and formal activation of the alternative pathway, and by activation of the classical and lectin pathways. If the deposited C3b is not appropriately regulated, there is progression to terminal pathway complement activation via the C5 convertases, generating the potent anaphylotoxin C5a and the membrane attack complex C5b-9. Unsurprisingly, these highly active components have the potential to cause injury to bystander host tissue, including the vascular endothelium. As such, complement activation on endothelium is normally tightly controlled by a large number of fluid-phase and membrane bound inhibitors, in an attempt to ensure that propagation of complement activation is appropriately restricted to invading pathogens and altered 'self', e.g. apoptotic and necrotic cells. The kidney is increasingly recognised as a site at particular risk from complement-mediated endothelial injury. Both genetic and acquired defects which impact on complement regulation predispose to this susceptibility. The thrombotic microangiopathy, haemolytic uraemic syndrome (HUS), will be used to illustrate the mechanisms by which the endothelial cell injury occurs. Finally, the underlying rationale for current and future potential therapeutic interventions in HUS and also the opportunities for enhancing endothelial defence to prevent relapsing disease through increased complement cytoprotective strategies will be summarised.
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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.