Evidence map›Paper›PMID 23553918›Full record

ArticleCell biochemistry and function2013

Carboxyl terminus of Hsp70-interacting protein (CHIP) is required to modulate cardiac hypertrophy and attenuate autophagy during exercise.

Monte S Willis, Jin-Na Min, Shaobin Wang, Holly McDonough, Pamela Lockyer, Kristine M Wadosky, Cam Patterson

Abstract read
In one paragraph

Article in Cell biochemistry and function, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

26 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. Relationship betweenJournal of thoracic disease · 2021
    Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Mechanical Regulation of Protein Translation in the Cardiovascular System.Frontiers in cell and developmental biology · 2020
    Review
  11. Article
  12. The role of heat shock proteins and co-chaperones in heart failure.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2018
    Review
  13. Article
  14. Exercise Decreases Marrow Adipose Tissue Through ß-Oxidation in Obese Running Mice.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2017
    Article
  15. Review
  16. Review
  17. Article
  18. The role of autophagy in cardiac hypertrophy.Acta biochimica et biophysica Sinica · 2016
    Review
  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

7 authors at 2 institutions in 1 country.

Monte S WillisMcAllister Heart Institute, University of North Carolina, Chapel Hill, NC, USA; Department of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill, NC, USA.
Jin-Na Min
Shaobin Wang
Holly McDonough
Pamela Lockyer
Kristine M Wadosky
Cam Patterson
University of North Carolina at Chapel Hill · USUniversity of North Carolina Health Care · US

Funding

CHIP: A link between the chaperone &proteasome systemsR01GM061728 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SCHISLER, JONATHAN C. · 2001 to 2013
$3.4M
Myocyte specific regulation of metabolism and the response to biomechanical forceR01HL104129 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI WILLIS, MONTE S · 2010 to 2018
$3.3M
NHLBI NIH HHS R01 HL104129NHLBI NIH HHS R01HL104129NIGMS NIH HHS R01 GM061728NIGMS NIH HHS R01GM061728
6 · The paper itself

Abstract

The carboxyl terminus of Hsp70-interacting protein (CHIP) is a ubiquitin ligase/cochaperone critical for the maintenance of cardiac function. Mice lacking CHIP (CHIP-/-) suffer decreased survival, enhanced myocardial injury and increased arrhythmias compared with wild-type controls following challenge with cardiac ischaemia reperfusion injury. Recent evidence implicates a role for CHIP in chaperone-assisted selective autophagy, a process that is associated with exercise-induced cardioprotection. To determine whether CHIP is involved in cardiac autophagy, we challenged CHIP-/- mice with voluntary exercise. CHIP-/- mice respond to exercise with an enhanced autophagic response that is associated with an exaggerated cardiac hypertrophy phenotype. No impairment of function was identified in the CHIP-/- mice by serial echocardiography over the 5 weeks of running, indicating that the cardiac hypertrophy was physiologic not pathologic in nature. It was further determined that CHIP plays a role in inhibiting Akt signalling and autophagy determined by autophagic flux in cardiomyocytes and in the intact heart. Taken together, cardiac CHIP appears to play a role in regulating autophagy during the development of cardiac hypertrophy, possibly by its role in supporting Akt signalling, induced by voluntary running in vivo.

Indexed as

AutophagyPhysical Conditioning, AnimalAnimalsCardiomegalyMiceMice, 129 StrainMice, Inbred C57BLProto-Oncogene Proteins c-aktSignal TransductionUbiquitin-Protein LigasesProto-Oncogene Proteins c-aktStub1 protein, mouseUbiquitin-Protein Ligasesautophagycardiac hypertrophyCHIPheartIGF-1 signallingubiquitin ligase

Identifiers

PMID23553918
PMCPMC3770741
OpenAlexW1905638251

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.