Evidence map›Paper›PMID 23775726›Full record

ReviewNeuromolecular medicine2013

SUMO and ischemic tolerance.

Yang-ja Lee, John M Hallenbeck

Abstract readReview
PubMed Publisher
In one paragraph

Review in Neuromolecular medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.9field-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

32 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Article
  3. SUMOtherapeutics for Ischemic Stroke.Pharmaceuticals (Basel, Switzerland) · 2023
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. SUMOylation as a Therapeutic Target for Myocardial Infarction.Frontiers in cardiovascular medicine · 2021
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Quantitative high-throughput screening identifies cytoprotective molecules that enhance SUMO conjugation via the inhibition of SUMO-specific protease (SENP)2.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
    Article
  17. Article
  18. Article
  19. Article
  20. 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

2 authors at 2 institutions in 1 country.

Yang-ja LeeStroke Branch, National Institute of Neurological Disease and Stroke, National Institutes of Health (NINDS/NIH), Bldg10/Rm5B06, MSC 1401, 10 Center Drive, Bethesda, MD, 20892, USA, wicknery@ninds.nih.gov.
John M Hallenbeck
National Institute of Neurological Disorders and Stroke · USNational Institutes of Health · US

Funding

Hibernation--a New Approach To Stroke TherapyZIANS002856 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI HALLENBECK, JOHN · 2009 to 2018
$9.9M
Intramural NIH HHS
6 · The paper itself

Abstract

Hibernating squirrels slow blood flow to a crawl, but sustain no damage to brain or other tissues. This phenomenon provides an excellent model of natural tolerance to ischemia. Small ubiquitin-like modifier (SUMO) is a 100-residue peptide that modifies other proteins by being attached to the epsilon amino group of specific lysine residues. The discovery of massive SUMOylation (by both SUMO-1 and SUMO-2/3) occurring in the brains of 13-lined ground squirrels (Ictidomys tridecemlineatus) during hibernation torpor had opened the door to the studies on SUMO and ischemic tolerance reviewed here. Ischemic stress was shown to increase the levels of SUMO conjugation, especially SUMO-2/3, mostly during reperfusion in animal models and during restoration of oxygen and glucose in cell culture systems. Over-expression or depletion of SUMOs and/or Ubc9 (the SUMO E2 conjugating enzyme) increases or decreases (respectively) the levels of SUMO conjugates. Elevated global SUMO conjugations were shown to cytoprotect from ischemic insults; conversely, depressed SUMOylation sensitized cells. Global protein conjugation not only by SUMOs, but also by other ubiquitin-like modifiers (ULMs) including NEDD8, ISG15, UFM1 and FUB1 was shown to be significantly increased in the brains of hibernating ground squirrels during torpor. These increases in multiple ULM conjugations may orchestrate the cellular events in hibernating ground squirrels that induce a state of natural tolerance through their multipronged effects. Certain miRNAs such as the miR-200 family and the miR-182 family were shown, at least partly, to control the levels of these ULM conjugations. Lowering the levels of these miRNAs leads to an increase in global SUMOylation/ULM conjugation, thereby providing the tolerance to ischemia. This suggests that these miRNAs may be good targets for therapeutic intervention in stroke.

Indexed as

AnimalsBrain IschemiaCells, CulturedCysteine EndopeptidasesDisease Models, AnimalGlucoseHibernationHumansHypothermiaHypothermia, InducedIschemiaMiceMice, TransgenicMicroRNAsModels, AnimalNerve Tissue ProteinsCysteine EndopeptidasesGlucoseMicroRNAsNerve Tissue ProteinsSmall Ubiquitin-Related Modifier ProteinsUbiquitinUbiquitin-Conjugating EnzymesUbiquitin-Conjugating Enzyme UBC9Ubiquitins

Identifiers

PMID23775726
OpenAlexW2071561335

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.