Evidence map›Paper›PMID 25659608›Full record

ReviewJournal of molecular medicine (Berlin, Germany)2015

Dynamin-related protein 1 as a therapeutic target in cardiac arrest.

Willard W Sharp

Open access · greenAbstract readReview
In one paragraph

Review in Journal of molecular medicine (Berlin, Germany), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 2 pooled it
2.9field-weighted citation impact, top 9% 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

31 citing papers in PubMed, 2 syntheses or guidelines pooled it, 62 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Targeting mitochondria to protect the heart: a matter of balance?Clinical science (London, England : 1979) · 2025
    Review
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  19. Molecular Machinery and Pathophysiology of Mitochondrial Dynamics.Frontiers in cell and developmental biology · 2021
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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

1 author at 1 institution in 1 country.

Willard W SharpSection of Emergency Medicine, Department of Medicine, University of Chicago, 5841 S. Maryland Ave, MC 5068, Chicago, IL, 60637, USA, wsharp@medicine.bsd.uchicago.edu.
University of Chicago · US

Funding

Re-Engineering Translational Research at the University of ChicagoUL1TR000430 · NCATS · UNIVERSITY OF CHICAGO · PI SOLWAY, JULIAN · 2012 to 2016
$20.2M
Hypothermia in Cardiac Arrest: Akt Preservation of Mitochondrial IntegrityK08HL103901 · NHLBI · UNIVERSITY OF CHICAGO · PI SHARP, WILLARD WILLIAM · 2011 to 2015
$633k
Mitochondrial dynamics in human pulmonary hypertension: a new therapeutic targetR03HL110826 · NHLBI · UNIVERSITY OF CHICAGO · PI SHARP, WILLARD WILLIAM · 2012 to 2013
$154k
NCATS NIH HHS UL1 TR000430NHLBI NIH HHS HL103901-01A1NHLBI NIH HHS K08 HL103901NHLBI NIH HHS R03 HL110826NHLBI NIH HHS R03 HL110826-01A1
6 · The paper itself

Abstract

Despite improvements in cardiopulmonary resuscitation (CPR) quality, defibrillation technologies, and implementation of therapeutic hypothermia, less than 10 % of out-of-hospital cardiac arrest (OHCA) victims survive to hospital discharge. New resuscitation therapies have been slow to develop, in part, because the pathophysiologic mechanisms critical for resuscitation are not understood. During cardiac arrest, systemic cessation of blood flow results in whole body ischemia. CPR and the restoration of spontaneous circulation (ROSC), both result in immediate reperfusion injury of the heart that is characterized by severe contractile dysfunction. Unlike diseases of localized ischemia/reperfusion (IR) injury (myocardial infarction and stroke), global IR injury of organs results in profound organ dysfunction with far shorter ischemic times. The two most commonly injured organs following cardiac arrest resuscitation, the heart and brain, are critically dependent on mitochondrial function. New insights into mitochondrial dynamics and the role of the mitochondrial fission protein Dynamin-related protein 1 (Drp1) in apoptosis have made targeting these mechanisms attractive for IR therapy. In animal models, inhibiting Drp1 following IR injury or cardiac arrest confers protection to both the heart and brain. In this review, the relationship of the major mitochondrial fission protein Drp1 to ischemic changes in the heart and its targeting as a new therapeutic target following cardiac arrest are discussed.

Indexed as

AnimalsCardiotonic AgentsDynaminsGTP PhosphohydrolasesHeart ArrestHumansMicrotubule-Associated ProteinsMitochondria, HeartMitochondrial DynamicsMitochondrial ProteinsMyocardial Reperfusion InjuryMyocardiumCardiotonic AgentsDNM1L protein, humanDynaminsGTP PhosphohydrolasesMicrotubule-Associated ProteinsMitochondrial Proteins

Identifiers

PMID25659608
PMCPMC4334717
OpenAlexW106888571

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.