Evidence map›Paper›PMID 26481155›Full record

ReviewPharmacology & therapeutics2015

Parkinson's disease proteins: Novel mitochondrial targets for cardioprotection.

Uma A Mukherjee, Sang-Bing Ong, Sang-Ging Ong, Derek J Hausenloy

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Pharmacology & therapeutics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 2 pooled it
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

39 citing papers in PubMed, 2 syntheses or guidelines pooled it, 81 citations in OpenAlex.

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  19. Alternative autophagy: mechanisms and roles in different diseases.Cell communication and signaling : CCS · 2022
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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

4 authors at 4 institutions in 3 countries.

Uma A MukherjeeThe Hatter Cardiovascular Institute, Institute of Cardiovascular Science, University College London, London, UK.
Sang-Bing OngCardiovascular and Metabolic Disorders Program, Duke-National University of Singapore, Singapore; National Heart Research Institute Singapore, National Heart Centre Singapore, Singapore.
Sang-Ging OngStanford Cardiovascular Institute, Stanford University School of Medicine, CA, USA.
Derek J HausenloyThe Hatter Cardiovascular Institute, Institute of Cardiovascular Science, University College London, London, UK; Cardiovascular and Metabolic Disorders Program, Duke-National University of Singapore, Singapore; National Heart Research Institute Singapore, National Heart Centre Singapore, Singapore; The National Institute of Health Research University College London Hospitals Biomedical Research Centre, London, UK. Electronic address: derek.hausenloy@duke-nus.edu.sg.
Cardiovascular Institute of the South · USNational University of Singapore · SGStanford University · USUniversity College London · GB

Funding

British Heart Foundation FS/09/060/28039British Heart Foundation FS/10/39/28270British Heart Foundation FS/13/41/30368Medical Research Council MR/J003530/1
6 · The paper itself

Abstract

Ischemic heart disease (IHD) is the leading cause of death and disability worldwide. Therefore, novel therapeutic targets for protecting the heart against acute ischemia/reperfusion injury (IRI) are required to attenuate cardiomyocyte death, preserve myocardial function, and prevent the onset of heart failure. In this regard, a specific group of mitochondrial proteins, which have been linked to familial forms of Parkinson's disease (PD), may provide novel therapeutic targets for cardioprotection. In dopaminergic neurons of the substantia nigra, these PD proteins, which include Parkin, PINK1, DJ-1, LRRK2, and α-synuclein, play essential roles in preventing cell death-through maintaining normal mitochondrial function, protecting against oxidative stress, mediating mitophagy, and preventing apoptosis. These rare familial forms of PD may therefore provide important insights into the pathophysiology underlying mitochondrial dysfunction and the development of PD. Interestingly, these PD proteins are also present in the heart, but their role in myocardial health and disease is not clear. In this article, we review the role of these PD proteins in the heart and explore their potential as novel mitochondrial targets for cardioprotection.

Indexed as

alpha-SynucleinCardiotonic AgentsCell DeathHumansIntracellular Signaling Peptides and ProteinsLeucine-Rich Repeat Serine-Threonine Protein Kinase-2MitochondriaMitophagyMyocardial IschemiaMyocardiumMyocytes, CardiacOncogene ProteinsOxidative StressParkinson DiseaseProtein Deglycase DJ-1Protein Kinasesalpha-SynucleinCardiotonic AgentsIntracellular Signaling Peptides and ProteinsLeucine-Rich Repeat Serine-Threonine Protein Kinase-2LRRK2 protein, humanOncogene ProteinsPARK7 protein, humanparkin proteinProtein Deglycase DJ-1Protein KinasesProtein Serine-Threonine KinasesPTEN-Induced Putative KinaseUbiquitin-Protein LigasesCoronary heart diseaseischaemic preconditioningmitochondriamyocardial ischaemia-reperfusion injuryParkinson’s disease

Identifiers

PMID26481155
PMCPMC4667215
OpenAlexW1947570107

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.