Evidence map›Paper›PMID 37791071›Full record

ReviewFrontiers in cell and developmental biology2023

Endothelial type I interferon response and brain diseases: identifying STING as a therapeutic target.

Nádia Duarte, Abdul Muktadir Shafi, Carlos Penha-Gonçalves, Teresa Faria Pais

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. The Ever-Expanding Influence of the Endothelial Nitric Oxide Synthase.Basic & clinical pharmacology & toxicology · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. 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

4 authors at 1 institution in 1 country.

Nádia DuarteInstituto Gulbenkian de Ciência, Oeiras, Portugal.
Abdul Muktadir ShafiInstituto Gulbenkian de Ciência, Oeiras, Portugal.
Carlos Penha-GonçalvesInstituto Gulbenkian de Ciência, Oeiras, Portugal.
Teresa Faria PaisInstituto Gulbenkian de Ciência, Oeiras, Portugal.
Instituto Gulbenkian de Ciência · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The endothelium layer lining the inner surface of blood vessels serves relevant physiological functions in all body systems, including the exchanges between blood and extravascular space. However, endothelial cells also participate in innate and adaptive immune response that contribute to the pathophysiology of inflammatory disorders. Type I Interferon (IFN) signaling is an inflammatory response triggered by a variety of pathogens, but it can also be induced by misplaced DNA in the cytosol caused by cell stress or gene mutations. Type I IFN produced by blood leukocytes or by the endothelium itself is well-known to activate the interferon receptor (IFNAR) in endothelial cells. Here, we discuss the induction of type I IFN secretion and signaling in the endothelium, specifically in the brain microvasculature where endothelial cells participate in the tight blood-brain barrier (BBB). This barrier is targeted during neuroinflammatory disorders such as infection, multiple sclerosis, Alzheimer's disease and traumatic brain injury. We focus on type I IFN induction through the cGAS-STING activation pathway in endothelial cells in context of autoinflammatory type I interferonopathies, inflammation and infection. By comparing the pathophysiology of two separate infectious diseases-cerebral malaria induced by

Indexed as

brainendothelial cellsinflammationSTINGtype I IFN

Identifiers

PMID37791071
PMCPMC10542901
OpenAlexW4386736455

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.