Evidence map›Paper›PMID 21756914›Full record

ArticleJournal of molecular and cellular cardiology2011

G protein coupled receptor kinase 2 interacting protein 1 (GIT1) is a novel regulator of mitochondrial biogenesis in heart.

Jinjiang Pang, Xiangbin Xu, Michael R Getman, Xi Shi, Stephen L Belmonte, Heidi Michaloski, Amy Mohan, Burns C Blaxall, Bradford C Berk

Abstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

14 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Macrophage GIT1 Contributes to Bone Regeneration by Regulating Inflammatory Responses in an ERK/NRF2-Dependent Way.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2020
    Article
  7. Article
  8. PGC1β Organizes the Osteoclast Cytoskeleton by Mitochondrial Biogenesis and Activation.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2018
    Article
  9. Review
  10. Review
  11. Review
  12. Key role of ERK1/2 molecular scaffolds in heart pathology.Cellular and molecular life sciences : CMLS · 2013
    Review
  13. Article
  14. 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

9 authors at 2 institutions in 1 country.

Jinjiang PangAab Cardiovascular Research Institute, Rochester, NY 14642, USA. Jinjiang_pang@URMC.rochester.edu
Xiangbin Xu
Michael R Getman
Xi Shi
Stephen L Belmonte
Heidi Michaloski
Amy Mohan
Burns C Blaxall
Bradford C Berk
Rochester Institute of Technology · USUniversity of Rochester Medical Center · US

Funding

ANGIOTENSIN II SIGNAL TRANSDUCTIONR01HL063462 · NHLBI · UNIVERSITY OF ROCHESTER · PI BERK, BRADFORD C · 1999 to 2012
$4.3M
NHLBI NIH HHS HL63462NHLBI NIH HHS R01 HL063462
6 · The paper itself

Abstract

G-protein-coupled receptor (GPCR)-kinase interacting protein-1 (GIT1) is a multi-function scaffold protein. However, little is known about its physiological role in the heart. Here we sought to identify the cardiac function of GIT1. Global GIT1 knockout (KO) mice were generated and exhibited significant cardiac hypertrophy that progressed to heart failure. Electron microscopy revealed that the hearts of GIT1 KO mice demonstrated significant morphological abnormities in mitochondria, including decreased mitochondrial volume density, cristae density and increased vacuoles. Moreover, mitochondrial biogenesis-related gene peroxisome proliferator-activated receptor γ (PPARγ) co-activator-1α (PGC-1α), PGC-1β, mitochondrial transcription factor A (Tfam) expression, and total mitochondrial DNA were remarkably decreased in hearts of GIT1 KO mice. These animals also had impaired mitochondrial function, as evidenced by reduced ATP production and dissipated mitochondrial membrane potential (Ψ(m)) in adult cardiomyocytes. Concordant with these mitochondrial observations, GIT1 KO mice showed enhanced cardiomyocyte apoptosis and cardiac dysfunction. In conclusion, our findings identify GIT1 as a new regulator of mitochondrial biogenesis and function, which is necessary for postnatal cardiac maturation.

Indexed as

Cell Cycle ProteinsGTPase-Activating ProteinsAdenosine TriphosphateAnimalsAnimals, NewbornApoptosisDNA-Binding ProteinsDNA, MitochondrialDown-RegulationHeart FailureMembrane Potential, MitochondrialMiceMice, KnockoutMicroscopy, ElectronMitochondria, HeartMitochondrial ProteinsAdenosine TriphosphateCell Cycle ProteinsDNA-Binding ProteinsDNA, MitochondrialGit1 protein, mouseGTPase-Activating ProteinsMitochondrial Proteinsmitochondrial transcription factor APeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPAR gammaPpargc1a protein, mouseTrans-ActivatorsTranscription Factors

Identifiers

PMID21756914
PMCPMC3367479
OpenAlexW2070955365

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.