Evidence map›Paper›PMID 32559654›Full record

ArticleBlood cells, molecules & diseases2020

Hypoxia induced up-regulation of tissue factor is mediated through extracellular RNA activated Toll-like receptor 3-activated protein 1 signalling.

Saumya Bhagat, Indranil Biswas, Rehan Ahmed, Gausal A Khan

Open access · greenAbstract read
In one paragraph

Article in Blood cells, molecules & diseases, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

18 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
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  10. Observational
  11. Article
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  13. COVID-19 Induced Coagulopathy (CIC): Thrombotic Manifestations of Viral Infection.TH open : companion journal to thrombosis and haemostasis · 2022
    Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Role of Tissue Factor in the Pathogenesis of COVID-19 and the Possible Ways to Inhibit It.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis
    Review
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

4 authors at 2 institutions in 2 countries.

Saumya BhagatDefence Institute of Physiology and Allied Sciences, Timarpur, Delhi, India.
Indranil BiswasDefence Institute of Physiology and Allied Sciences, Timarpur, Delhi, India.
Rehan AhmedArmy Hospital Research and Referral, Delhi, India.
Gausal A KhanDefence Institute of Physiology and Allied Sciences, Timarpur, Delhi, India; Department of Physiology and Physiotherapy, CMNHS, Fiji National University, Suva, Fiji Islands. Electronic address: gausalk@gmail.com.
Defence Institute of Physiology and Allied Sciences · INArmy Hospital Research and Referral · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sterile Inflammation (SI), a condition where damage associated molecular patterns (DAMPs) released from dying cells, leads to TLR (Toll-like receptor) activation and triggers hypoxemia in circulation leading to venous thrombosis (VT) through tissue factor (TF) activation, but its importance under acute hypoxia (AH) remains unexplored. Thus, we hypothesized that eRNA released from dying cells under AH activates TF via the TLR3-ERK1/2-AP1 pathway, leading to VT. Animals were exposed to stimulate hypoxia for 0-24 h at standard temperature and humidity. RNaseA and DNase1 were injected immediately before exposure. TLR3 gene silencing was performed through in vivo injection of TLR3 siRNA. 80 μg/kg BW of isolated eRNA and eDNA were injected 6 h prior to sacrifice. Antigens of TF pathway were determined by ELISA and TF activity by a chromogenic assay. AH exposure significantly induced release of SI markers i.e. eRNA, eDNA, HMGB1 and upregulated TLR3, ERK1/2 (Extracellular signal-regulated kinases), AP1 (Activator Protein-1) and TF, whereas RNaseA pre-treatment diminished the effect of AH, thus inhibiting TF expression as well as activity during AH. Hence, we propose a possible mechanism of AH-induced TF activation and thrombosis where RNaseA can become the novel focal point in ameliorating therapy for AH induced thrombosis.

Indexed as

Signal TransductionAnimalsCells, CulturedHypoxiaMAP Kinase Signaling SystemMiceReplication Protein CRNAThromboplastinThrombosisToll-Like Receptor 3Up-RegulationReplication Protein CRNAThromboplastinTLR3 protein, mouseToll-Like Receptor 3HypoxiaSterile InflammationThrombosisTissue factorTLR3

Identifiers

PMID32559654
PMCPMC7287429
OpenAlexW3035482029

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.