ArticleJournal of cellular and molecular medicine2015
Complement inhibition decreases early fibrogenic events in the lung of septic baboons.
Article in Journal of cellular and molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
28 citing papers in PubMed, 39 citations in OpenAlex.
- Effect of antibody-mediated connective tissue growth factor neutralization on lung edema in ventilator-induced lung injury in rats.Molecular medicine (Cambridge, Mass.) · 2024Article
- Complement System Inhibitory Drugs in a Zebrafish (International journal of molecular sciences · 2023Article
- Complement and COVID-19: Three years on, what we know, what we don't know, and what we ought to know.Immunobiology · 2023Review
- Complement as a vital nexus of the pathobiological connectome for acute respiratory distress syndrome: An emerging therapeutic target.Frontiers in immunology · 2023Review
- Overexpression of Decay Accelerating Factor Mitigates Fibrotic Responses to Lung Injury.American journal of respiratory cell and molecular biology · 2022Article
- Complement 3a Mediates CCN2/CTGF in Human Retinal Pigment Epithelial Cells.Journal of ophthalmology · 2022Article
- Complement as driver of systemic inflammation and organ failure in trauma, burn, and sepsis.Seminars in immunopathology · 2021Review
- Disease-drug and drug-drug interaction in COVID-19: Risk and assessment.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021Review
- Complement Inhibition and COVID-19: The Story so Far.ImmunoTargets and therapy · 2021Review
- D-Limonene Is a Potential Monoterpene to Inhibit PI3K/Akt/IKK-α/NF-κB p65 Signaling Pathway in Coronavirus Disease 2019 Pulmonary Fibrosis.Frontiers in medicine · 2021Article
- Mitofusion 2 Overexpression Decreased Proliferation of Human Embryonic Lung Fibroblasts in Acute Respiratory Distress Syndrome through Inhibiting RAS-RAF-1-ERK1/2 Pathway.Current medical science · 2020Article
- The role of endothelial shear stress on haemodynamics, inflammation, coagulation and glycocalyx during sepsis.Journal of cellular and molecular medicine · 2020Review
- Computational analysis of complement inhibitor compstatin using molecular dynamics.Journal of molecular modeling · 2020Article
- S1P lyase inhibition protects against sepsis by promoting disease tolerance via the S1P/S1PR3 axis.EBioMedicine · 2020Observational
- The first case of COVID-19 treated with the complement C3 inhibitor AMY-101.Clinical immunology (Orlando, Fla.) · 2020Article
- Nonhuman primate species as models of human bacterial sepsis.Lab animal · 2019Review
- Protective Effects of the Complement Inhibitor Compstatin CP40 in Hemorrhagic Shock.Shock (Augusta, Ga.) · 2019Article
- Safety profile after prolonged C3 inhibition.Clinical immunology (Orlando, Fla.) · 2018Article
- IL-17A deficiency mitigates bleomycin-induced complement activation during lung fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- Inhibition of complement C5 protects against organ failure and reduces mortality in a baboon model ofProceedings of the National Academy of Sciences of the United States of America · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
Acute respiratory distress syndrome (ARDS) induced by severe sepsis can trigger persistent inflammation and fibrosis. We have shown that experimental sepsis in baboons recapitulates ARDS progression in humans, including chronic inflammation and long-lasting fibrosis in the lung. Complement activation products may contribute to the fibroproliferative response, suggesting that complement inhibitors are potential therapeutic agents. We have been suggested that treatment of septic baboons with compstatin, a C3 convertase inhibitor protects against ARDS-induced fibroproliferation. Baboons challenged with 10(9) cfu/kg (LD50) live E. coli by intravenous infusion were treated or not with compstatin at the time of challenge or 5 hrs thereafter. Changes in the fibroproliferative response at 24 hrs post-challenge were analysed at both transcript and protein levels. Gene expression analysis showed that sepsis induced fibrotic responses in the lung as early as 24 hrs post-bacterial challenge. Immunochemical and biochemical analysis revealed enhanced collagen synthesis, induction of profibrotic factors and increased cell recruitment and proliferation. Specific inhibition of complement with compstatin down-regulated sepsis-induced fibrosis genes, including transforming growth factor-beta (TGF-β), connective tissue growth factor (CTGF), tissue inhibitor of metalloproteinase 1 (TIMP1), various collagens and chemokines responsible for fibrocyte recruitment (e.g. chemokine (C-C motif) ligand 2 (CCL2) and 12 (CCL12)). Compstatin decreased the accumulation of myofibroblasts and proliferating cells, reduced the production of fibrosis mediators (TGF-β, phospho-Smad-2 and CTGF) and inhibited collagen deposition. Our data demonstrate that complement inhibition effectively attenuates collagen deposition and fibrotic responses in the lung after severe sepsis. Inhibiting complement could prove an attractive strategy for preventing sepsis-induced fibrosis of the lung.
Indexed as
Identifiers
What OpenQuestion holds
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.