Evidence map›Paper›PMID 28900700›Full record

ReviewSeminars in immunopathology2018

Auxiliary activation of the complement system and its importance for the pathophysiology of clinical conditions.

Markus Huber-Lang, Kristina N Ekdahl, Rebecca Wiegner, Karin Fromell, Bo Nilsson

Open access · hybridAbstract readReview
In one paragraph

Review in Seminars in immunopathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-weighted citation impact, top 13% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
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  5. Frontiers in cellular and infection microbiology · 2023
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

Markus Huber-LangInstitute of Clinical and Experimental Trauma-Immunology, University Hospital Ulm, 89081, Ulm, Germany.
Kristina N EkdahlDepartment of Immunology, Genetics and Pathology (IGP), Rudbeck Laboratory C5:3, Uppsala University, SE-751 85, Uppsala, Sweden.
Rebecca WiegnerInstitute of Clinical and Experimental Trauma-Immunology, University Hospital Ulm, 89081, Ulm, Germany.
Karin FromellDepartment of Immunology, Genetics and Pathology (IGP), Rudbeck Laboratory C5:3, Uppsala University, SE-751 85, Uppsala, Sweden.
Bo NilssonDepartment of Immunology, Genetics and Pathology (IGP), Rudbeck Laboratory C5:3, Uppsala University, SE-751 85, Uppsala, Sweden. Bo.Nilsson@igp.uu.se.
Uppsala University · SEUniversity Hospital Ulm · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activation and regulation of the cascade systems of the blood (the complement system, the coagulation/contact activation/kallikrein system, and the fibrinolytic system) occurs via activation of zymogen molecules to specific active proteolytic enzymes. Despite the fact that the generated proteases are all present together in the blood, under physiological conditions, the activity of the generated proteases is controlled by endogenous protease inhibitors. Consequently, there is remarkable little crosstalk between the different systems in the fluid phase. This concept review article aims at identifying and describing conditions where the strict system-related control is circumvented. These include clinical settings where massive amounts of proteolytic enzymes are released from tissues, e.g., during pancreatitis or post-traumatic tissue damage, resulting in consumption of the natural substrates of the specific proteases and the available protease inhibitor. Another example of cascade system dysregulation is disseminated intravascular coagulation, with canonical activation of all cascade systems of the blood, also leading to specific substrate and protease inhibitor elimination. The present review explains basic concepts in protease biochemistry of importance to understand clinical conditions with extensive protease activation.

Indexed as

AnimalsComplement ActivationComplement C3-C5 Convertases, Classical PathwayComplement System ProteinsDisease SusceptibilityEnzyme ActivationHumansKineticsMolecular Targeted TherapyPeptide HydrolasesProtease InhibitorsProtein BindingProteolysisSignal TransductionSubstrate SpecificityComplement C3-C5 Convertases, Classical PathwayComplement System ProteinsPeptide HydrolasesProtease InhibitorsComplement systemProtease inhibitorsProteasesTrauma

Identifiers

PMID28900700
PMCPMC5794838
OpenAlexW2754796549

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.