Evidence map›Paper›PMID 29214442›Full record

ReviewPediatric nephrology (Berlin, Germany)2019

Shiga toxin triggers endothelial and podocyte injury: the role of complement activation.

Carlamaria Zoja, Simona Buelli, Marina Morigi

Abstract readReview
PubMed Publisher
In one paragraph

Review in Pediatric nephrology (Berlin, Germany), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

26 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
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  3. Severe glomerular fibrin thrombosis in a dog.The Journal of veterinary medical science · 2024
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  19. Cerebral sinovenous thrombosis in pediatric hemolytic uremic syndrome.Research and practice in thrombosis and haemostasis · 2020
    Article
  20. Article
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

3 authors at 1 institution in 1 country.

Carlamaria ZojaCentro Anna Maria Astori, Science and Technology Park Kilometro Rosso, IRCCS - Istituto di Ricerche Farmacologiche "Mario Negri", Via Stezzano, 87, 24126, Bergamo, Italy. carlamaria.zoja@marionegri.it.
Simona BuelliCentro Anna Maria Astori, Science and Technology Park Kilometro Rosso, IRCCS - Istituto di Ricerche Farmacologiche "Mario Negri", Via Stezzano, 87, 24126, Bergamo, Italy.
Marina MorigiCentro Anna Maria Astori, Science and Technology Park Kilometro Rosso, IRCCS - Istituto di Ricerche Farmacologiche "Mario Negri", Via Stezzano, 87, 24126, Bergamo, Italy.
Mario Negri Institute for Pharmacological Research · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Shiga toxin (Stx)-producing Escherichia coli (STEC) is the offending agent in post-diarrhea-associated hemolytic uremic syndrome (HUS), a disorder characterized by thrombocytopenia, microangiopathic hemolytic anemia, and acute kidney failure, with thrombi occluding the renal microvasculature. Endothelial dysfunction has been recognized as the trigger event in the development of microangiopathic processes. Glomerular endothelial cells are susceptible to the toxic effects of Stxs that, via nuclear factor kappa B (NF-κB) activation, induce the expression of genes encoding for adhesion molecules and chemokines, culminating in leukocyte adhesion and platelet thrombus formation on the activated endothelium. Complement activation via the alternative pathway has been seen in patients during the acute phase of STEC-associated HUS. Experimental evidence has highlighted the role of complement proteins in driving glomerular endothelium toward a thrombogenic phenotype. At the glomerular level, podocytes are also an important target of Stx-induced complement activation. Glomerular injury as a consequence of podocyte dysfunction and loss is thus a mechanism that might affect long-term renal outcomes in the disease. New approaches to targeting the complement system may be useful therapeutic options for patients with STEC-HUS.

Indexed as

AnimalsColonComplement Pathway, AlternativeDiarrheaDisease Models, AnimalEndothelial CellsHemolytic-Uremic SyndromeHumansImmunosuppressive AgentsIntestinal MucosaMicrovesselsPodocytesShiga-Toxigenic Escherichia coliShiga ToxinImmunosuppressive AgentsShiga ToxinComplement alternative pathwayEndothelial injuryEnterohemorrhagic Escherichia coliHemolytic uremic syndromeMicrovascular thrombosisPodocytesShiga toxin

Identifiers

PMID29214442
OpenAlexW2771325834

What OpenQuestion holds

Textmetadata
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.