Evidence map›Paper›PMID 24400695›Full record

ArticleAmerican journal of respiratory cell and molecular biology2014

IL-1α reversibly inhibits skeletal muscle ryanodine receptor. a novel mechanism for critical illness myopathy?

Oliver Friedrich, Bing Yi, Joshua N Edwards, Barbara Reischl, Anette Wirth-Hücking, Andreas Buttgereit, Roland Lang, Cornelia Weber, Fabian Polyak, Ilon Liu and 5 more

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2014. 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 14% 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, 30 citations in OpenAlex.

  1. Article
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  3. Review
  4. Article
  5. Article
  6. Pathophysiology and management of critical illness polyneuropathy and myopathy.Journal of applied physiology (Bethesda, Md. : 1985) · 2021
    Article
  7. Article
  8. Review
  9. Article
  10. Epinephrine stimulates CXCL1 IL-1Physiological reports · 2017
    Article
  11. Article
  12. Cannabinoid signalling inhibits sarcoplasmic CaThe Journal of physiology · 2016
    Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. 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

15 authors at 4 institutions in 2 countries.

Oliver Friedrich1 Institute of Medical Biotechnology, Friedrich-Alexander-University Erlangen-Nuremberg, Erlangen, Germany.
Bing Yi
Joshua N Edwards
Barbara Reischl
Anette Wirth-Hücking
Andreas Buttgereit
Roland Lang
Cornelia Weber
Fabian Polyak
Ilon Liu
Frederic von Wegner
Tanya R Cully
Aven Lee
Patrick Most
Mirko Völkers
Heidelberg University · DEFriedrich-Alexander-Universität Erlangen-Nürnberg · DEThe University of Queensland · AUGoethe University Frankfurt · DE

Funding

S100A1: A Novel Modulator of Myocardial Infarct Inflammation and RegenerationR01HL092130 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI PEPPEL, KARSTEN · 2008 to 2012
$2.2M
NHLBI NIH HHS R01 HL092130NHLBI NIH HHS R01 HL92130NHLBI NIH HHS R01 HL92130-2S1
6 · The paper itself

Abstract

Critical illness myopathies in patients with sepsis or sustained mechanical ventilation prolong intensive care treatment and threaten both patients and health budgets; no specific therapy is available. Underlying pathophysiological mechanisms are still patchy. We characterized IL-1α action on muscle performance in "skinned" muscle fibers using force transducers and confocal Ca(2+) fluorescence microscopy for force/Ca(2+) transients and Ca(2+) sparks. Association of IL-1α with sarcoplasmic reticulum (SR) release channel, ryanodine receptor (RyR) 1, was investigated with coimmunoprecipitation and confocal immunofluorescence colocalization. Membrane integrity was studied in single, intact fibers challenged with IL-1α. IL-1α reversibly stabilized Mg(2+) inhibition of Ca(2+) release. Low Mg(2+)-induced force and Ca(2+) transients were reversibly abolished by IL-1α. At normal Mg(2+), IL-1α reversibly increased caffeine-induced force and Ca(2+) transients. IL-1α reduced SR Ca(2+) leak via RyR1, as judged by (1) increased SR Ca(2+) retention, (2) increased IL-1α force transients being reproduced by 25 μM tetracaine, and (3) reduced Ca(2+) spark frequencies by IL-1α or tetracaine. Coimmunoprecipitation confirmed RyR1/IL-1 association. RyR1/IL-1 immunofluorescence patterns perfectly colocalized. Long-term, 8-hour IL-1α challenge of intact muscle fibers compromised membrane integrity in approximately 50% of fibers, and confirmed intracellular IL-1α deposition. IL-1α exerts a novel, specific, and reversible interaction mechanism with the skeletal muscle RyR1 macromolecular release complex without the need to act via its membrane IL-1 receptor, as IL-1R membrane expression levels were not detectable in Western blots or immunostaining of single fibers. We present a potential explanation of how the inflammatory mediator, IL-1α, may contribute to muscle weakness in critical illness.

Indexed as

AnimalsCalciumCell MembraneCritical IllnessInterleukin-1MagnesiumMiceMice, Inbred C57BLMuscle Fibers, SkeletalMuscle WeaknessMuscular DiseasesProtein BindingRyanodine Receptor Calcium Release ChannelSarcoplasmic ReticulumCalciumInterleukin-1MagnesiumRyanodine Receptor Calcium Release Channel

Identifiers

PMID24400695
PMCPMC4068910
OpenAlexW2083937009

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.