Evidence map›Paper›PMID 21511881›Full record

ReviewMolecular endocrinology (Baltimore, Md.)2011

Minireview: Glucocorticoids in autoimmunity: unexpected targets and mechanisms.

Jamie R Flammer, Inez Rogatsky

Abstract readReview
In one paragraph

Review in Molecular endocrinology (Baltimore, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
7.0field-weighted citation impact, top 2% 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

65 citing papers in PubMed, 138 citations in OpenAlex.

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  19. Glucocorticoid-Dependent Mechanisms of Brain Tolerance to Hypoxia.International journal of molecular sciences · 2021
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5 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Jamie R FlammerHospital for Special Surgery Research Division, Weill Cornell Graduate School of Medical Sciences, New York, New York 10021, USA.
Inez Rogatsky
Hospital for Special Surgery · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

For decades, natural and synthetic glucocorticoids (GC) have been among the most commonly prescribed classes of immunomodulatory drugs. Their unsurpassed immunosuppressive and antiinflammatory activity along with cost-effectiveness makes these compounds a treatment of choice for the majority of autoimmune and inflammatory diseases, despite serious side effects that frequently accompany GC therapy. The activated GC receptor (GR) that conveys the signaling information of these steroid ligands to the transcriptional machinery engages a number of pathways to ultimately suppress autoimmune responses. Of those, GR-mediated apoptosis of numerous cell types of hematopoietic origin and suppression of proinflammatory cytokine gene expression have been described as the primary mechanisms responsible for the antiinflammatory actions of GC. However, along with the ever-increasing appreciation of the complex functions of the immune system in health and disease, we are beginning to recognize new facets of GR actions in immune cells. Here, we give a brief overview of the extensive literature on the antiinflammatory activities of GC and discuss in greater detail the unexpected pathways, factors, and mechanisms that have recently begun to emerge as novel targets for GC-mediated immunosuppression.

Indexed as

AutoimmunityAnimalsGlucocorticoidsHumansInterferon Type ILymphocyte ActivationReceptors, GlucocorticoidSignal TransductionSTAT Transcription FactorsT-Lymphocytes, Helper-InducerGlucocorticoidsInterferon Type IReceptors, GlucocorticoidSTAT Transcription Factors

Identifiers

PMID21511881
PMCPMC5417249
OpenAlexW2021846928

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.