ReviewSpringer seminars in immunopathology2005
Emission of membrane vesicles: roles in complement resistance, immunity and cancer.
Review in Springer seminars in immunopathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 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.
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Who cites it
86 citing papers in PubMed, 194 citations in OpenAlex.
- 3'-Sialyllactose Prevents Atherosclerosis by Attenuating Chronic Inflammation via the Gut-Immune-Cardiovascular Axis inFood science & nutrition · 2026Article
- Complement C4b and factor B in astrocyte-derived exosomes as novel biomarkers for amnestic mild cognitive impairment.Frontiers in aging neuroscience · 2026Article
- Plant-Derived Nanovesicle Enhanced Microribonucleic Acid (MicroRNA) Transfer from Nasal Cavity to the Brain.Molecular pharmaceutics · 2025Article
- 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
- Aberrant Lipid Metabolism and Complement Activation in Age-Related Macular Degeneration.Investigative ophthalmology & visual science · 2024Review
- Quantitative Analysis of Complement Membrane Attack Complex Proteins Associated with Extracellular Vesicles.Proteomes · 2024Article
- Extracellular Vesicles in the Pathogenesis, Clinical Characterization, and Management of Dermatomyositis: A Narrative Review.International journal of molecular sciences · 2024Review
- Diversity of extracellular HSP70 in cancer: advancing from a molecular biomarker to a novel therapeutic target.Frontiers in oncology · 2024Review
- Terminal complement complex deposition on chondrocytes promotes premature senescence in age- and trauma-related osteoarthritis.Frontiers in immunology · 2024Article
- Extracellular Vesicles and Hepatocellular Carcinoma: Opportunities and Challenges.Frontiers in oncology · 2022Review
- Conventional and Nonconventional Sources of Exosomes-Isolation Methods and Influence on Their Downstream Biomedical Application.Frontiers in molecular biosciences · 2022Review
- Proteome changes of plasma-derived extracellular vesicles in patients with myelodysplastic syndrome.PloS one · 2022Article
- Extracellular vesicle-mediated transport: Reprogramming a tumor microenvironment conducive with breast cancer progression and metastasis.Translational oncology · 2022Review
- Complement as driver of systemic inflammation and organ failure in trauma, burn, and sepsis.Seminars in immunopathology · 2021Review
- Small extracellular vesicles in cancer.Bioactive materials · 2021Review
- Beyond pore formation: reorganization of the plasma membrane induced by pore-forming proteins.Cellular and molecular life sciences : CMLS · 2021Review
- Review
- Investigation of the Molecular Mechanisms of Antioxidant Damage and Immune Response Downregulation in Liver ofFrontiers in endocrinology · 2021Article
- Is It Possible to Intervene in the Capacity ofFrontiers in immunology · 2021Review
- Extracellular vesicles: novel communicators in lung diseases.Respiratory research · 2020Review
26 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Complement-mediated cell death is caused by C5b-9, the membrane attack complex (MAC) composed of the five complement proteins C5b, C6, C7, C8, and C9. Assembly of the C5b-9 complex initiates oligomerization of C9 and production of a transmembrane protein channel that inflicts damage to target cells. For protection, cells eliminate the MAC from their surface either by ectocytosis (direct emission of membrane vesicles) or by endocytosis (internalization). The process of ectosome release is rapid and involves cytosolic Ca(2+) and activation of protein kinases, such as protein kinase C (PKC) and extracellular signal-regulated protein kinase (ERK). Recently, the involvement of mortalin (also known as GRP75 and mitochondrial hsp70) in MAC elimination has been suggested. Extracellular application of antibodies directed to mortalin increases cell sensitivity to MAC-mediated lysis. Release of membrane vesicles is ubiquitous and enhanced in apoptotic or tumor cells and upon cell activation. Composition of the ectosomes (also often referred to as microparticles) membrane proteins and lipids appears to be different from those of the original plasma membrane, indicating involvement of a selective sorting process during ectosome formation. Exosomes (unlike ectosomes) are membrane vesicles generated by endocytosis, endosome sorting into perinuclear multivesicular bodies (MVB) and exocytosis of MVBs. Exosomes appear to be different in size and composition from ectosomes. Exosome-associated MAC has also been described. Although research on ectosomes and exosomes is still limited, physiological roles in coagulation, vascular functions, angiogenesis, wound healing and development have been attributed to these shed membrane vesicles. On the other hand, there are indications that elevated levels of ectosomes and exosomes may predispose to morbidity. Membrane vesicles released by cells exposed to complement MAC may play roles in health and disease beyond protection from cell death.
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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.