Evidence map›Paper›PMID 22710345›Full record

ReviewThe international journal of biochemistry & cell biology2012

Small heat shock proteins in redox metabolism: implications for cardiovascular diseases.

Elisabeth S Christians, Takahiro Ishiwata, Ivor J Benjamin

Abstract readReview
In one paragraph

Review in The international journal of biochemistry & cell biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

38 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Proteostasis in cardiac health and disease.Nature reviews. Cardiology · 2017
    Review
  18. Article
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

Elisabeth S ChristiansLaboratory of Cardiac Disease, Redox Signaling and Cell Regeneration, Division of Cardiology, University of Utah School of Medicine, Salt Lake City, UT 84132, USA. ec1402@yahoo.com
Takahiro Ishiwata
Ivor J Benjamin
University of Utah · US

Funding

Protein Misfolding Diseases and Oxido-Reductive PathwaysDP1OD006438 · OD · UNIVERSITY OF UTAH · PI BENJAMIN, IVOR JAMES · 2009 to 2011
$2.2M
Reductive Stress in the Pathogenesis of R120GCryAB CardiomyopathyR01HL063834 · NHLBI · UNIVERSITY OF UTAH · PI BENJAMIN, IVOR JAMES · 2000 to 2010
$2.2M
Mechanisms of HSPB2 in Cardiac Metabolism and Ischemic CardioprotectionR01HL074370 · NHLBI · UNIVERSITY OF UTAH · PI BENJAMIN, IVOR JAMES · 2008 to 2011
$1.5M
Protein Misfolding Diseases and Oxido-Reductive PathwaysDP1HL117650 · NHLBI · UNIVERSITY OF UTAH · PI BENJAMIN, IVOR JAMES · 2012 to 2013
$1.5M
NHLBI NIH HHS 2 R01 HL063834-06NHLBI NIH HHS 5R01HL074370-03NHLBI NIH HHS DP1 HL117650NHLBI NIH HHS R01 HL063834NHLBI NIH HHS R01 HL074370NIH HHS 1DP1OD006438-02NIH HHS DP1 OD006438
6 · The paper itself

Abstract

A timely review series on small heat shock proteins has to appropriately examine their fundamental properties and implications in the cardiovascular system since several members of this chaperone family exhibit robust expression in the myocardium and blood vessels. Due to energetic and metabolic demands, the cardiovascular system maintains a high mitochondrial activity but irreversible oxidative damage might ensue from increased production of reactive oxygen species. How equilibrium between their production and scavenging is achieved becomes paramount for physiological maintenance. For example, heat shock protein B1 (HSPB1) is implicated in maintaining this equilibrium or redox homeostasis by upholding the level of glutathione, a major redox mediator. Studies of gain or loss of function achieved by genetic manipulations have been highly informative for understanding the roles of those proteins. For example, genetic deficiency of several small heat shock proteins such as HSPB5 and HSPB2 is well-tolerated in heart cells whereas a single missense mutation causes human pathology. Such evidence highlights both the profound genetic redundancy observed among the multigene family of small heat shock proteins while underscoring the role proteotoxicity plays in driving disease pathogenesis. We will discuss the available data on small heat shock proteins in the cardiovascular system, redox metabolism and human diseases. From the medical perspective, we envision that such emerging knowledge of the multiple roles small heat shock proteins exert in the cardiovascular system will undoubtedly open new avenues for their identification and possible therapeutic targeting in humans. This article is part of a Directed Issue entitled: Small HSPs in physiology and pathology.

Indexed as

Oxidative StressAnimalsCardiovascular DiseasesCardiovascular SystemGene Expression Regulation, DevelopmentalHeat-Shock Proteins, SmallHumansMutationOxidation-ReductionProteostasis DeficienciesHeat-Shock Proteins, Small

Identifiers

PMID22710345
PMCPMC3412898
OpenAlexW2058328743

What OpenQuestion holds

Textmetadata
LicenceTDM
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.