Evidence map›Paper›PMID 26992930›Full record

ReviewBiochimica et biophysica acta2016

Central Parkin: The evolving role of Parkin in the heart.

Gerald W Dorn

Abstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

17 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Activation of CaCell death and differentiation · 2024
    Article
  7. Article
  8. Article
  9. Article
  10. Mitofusins as mitochondrial anchors and tethers.Journal of molecular and cellular cardiology · 2020
    Review
  11. Article
  12. Review
  13. Autonomic dysfunction in Parkinson disease and animal models.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2019
    Review
  14. Article
  15. Decrease of Cardiac Parkin Protein in Obese Mice.Frontiers in cardiovascular medicine · 2019
    Article
  16. Article
  17. 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

1 author at 1 institution in 1 country.

Gerald W DornCenter for Pharmacogenomics, Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO, United States. Electronic address: gdorn@dom.wustl.edu.
Washington University in St. Louis · US

Funding

MOLECULAR MECHANISM OF APOPTOTIC CARDIOMYOPATHYR01HL059888 · NHLBI · WASHINGTON UNIVERSITY · PI DORN, GERALD W. · 1999 to 2016
$5.4M
G-Protein Receptor Kinases in Cardiac Stress AdaptationR01HL087871 · NHLBI · WASHINGTON UNIVERSITY · PI DORN, GERALD W. · 2007 to 2016
$4.1M
Linking cell death and mitochondrial quality control mechanisms in heart diseaseR01HL128071 · NHLBI · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI DORN, GERALD W., KITSIS, RICHARD N · 2015 to 2018
$2.1M
MICRORNA TARGETING IN HEART FAILURER01HL108943 · NHLBI · WASHINGTON UNIVERSITY · PI DORN, GERALD W. · 2012 to 2015
$1.5M
MOLECULAR ORCHESTRATION OF MITOCHONDRIAL FITNESS VIA REPLACEMENT OR REPAIRR01HL128441 · NHLBI · WASHINGTON UNIVERSITY · PI DORN, GERALD W. · 2016 to 2016
$381k
NHLBI NIH HHS R01 HL059888NHLBI NIH HHS R01 HL087871NHLBI NIH HHS R01 HL108943NHLBI NIH HHS R01 HL128071NHLBI NIH HHS R01 HL128441NHLBI NIH HHS R01 HL87871
6 · The paper itself

Abstract

Parkin is familiar to many because of its link to Parkinson's disease, and to others because of its well-characterized role as a central factor mediating selective mitophagy of damaged mitochondria for mitochondrial quality control. The genetic connection between Parkin and Parkinson's disease derives from clinical gene-association studies, whereas our mechanistic understanding of Parkin functioning in mitophagy is based almost entirely on work performed in cultured cells. Surprisingly, experimental evidence linking the disease and the presumed mechanism derives almost entirely from fruit flies; germline Parkin deficient mice do not develop Parkinson's disease phenotypes. Moreover, genetic manipulation of Parkin signaling in mouse hearts does not support a central role for Parkin in homeostatic mitochondrial quality control in this mitochondria-rich and -dependent organ. Here, I provide an overview of data suggesting that (in mouse hearts at least) Parkin functions more as a stress-induced and developmentally-programmed facilitator of cardiomyocyte mitochondrial turnover. This article is part of a Special Issue entitled 'EBEC 2016: 19th European Bioenergetics Conference, Riva del Garda, Italy, July 2-6, 2016.

Indexed as

AnimalsDisease Models, AnimalDrosophila melanogasterDynaminsGene Expression RegulationGTP PhosphohydrolasesHumansMiceMice, KnockoutMitochondria, HeartMitochondrial ProteinsMitophagyMyocardial InfarctionMyocardiumMyocytes, CardiacParkinson DiseaseDnm1l protein, mouseDynaminsGTP PhosphohydrolasesMFN2 protein, humanMitochondrial Proteinsparkin proteinProtein KinasesPTEN-Induced Putative KinaseUbiquitin-Protein Ligases

Identifiers

PMID26992930
PMCPMC4893897
OpenAlexW2297188206

What OpenQuestion holds

Textmetadata
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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.