Evidence map›Paper›PMID 30009835›Full record

ReviewNeuropharmacology2019

Aiming for the target: Mitochondrial drug delivery in traumatic brain injury.

Andrew M Lamade, Elizabeth M Kenny, Tamil S Anthonymuthu, Elif Soysal, Robert S B Clark, Valerian E Kagan, Hülya Bayır

Abstract readReview
In one paragraph

Review in Neuropharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
–field-weighted citation impact
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

24 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Regional NeurodegenerationFrontiers in computational neuroscience · 2021
    Article
  14. Article
  15. Review
  16. RepositioningPharmaceutics · 2020
    Article
  17. Review
  18. Article
  19. Review
  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.

Andrew M LamadeDepartment of Critical Care Medicine, Safar Center for Resuscitation Research, Children's Hospital of Pittsburgh, Pittsburgh, PA, USA; Department of Environmental and Occupational Health, Center for Free Radical and Antioxidant Health, University of Pittsburgh, Pittsburgh, PA, USA.
Elizabeth M KennyDepartment of Critical Care Medicine, Safar Center for Resuscitation Research, Children's Hospital of Pittsburgh, Pittsburgh, PA, USA; Department of Environmental and Occupational Health, Center for Free Radical and Antioxidant Health, University of Pittsburgh, Pittsburgh, PA, USA.
Tamil S AnthonymuthuDepartment of Critical Care Medicine, Safar Center for Resuscitation Research, Children's Hospital of Pittsburgh, Pittsburgh, PA, USA; Department of Environmental and Occupational Health, Center for Free Radical and Antioxidant Health, University of Pittsburgh, Pittsburgh, PA, USA.
Elif SoysalDepartment of Critical Care Medicine, Safar Center for Resuscitation Research, Children's Hospital of Pittsburgh, Pittsburgh, PA, USA.
Robert S B ClarkDepartment of Critical Care Medicine, Safar Center for Resuscitation Research, Children's Hospital of Pittsburgh, Pittsburgh, PA, USA.
Valerian E KaganDepartment of Environmental and Occupational Health, Center for Free Radical and Antioxidant Health, University of Pittsburgh, Pittsburgh, PA, USA; Laboratory of Navigational Redox Lipidomics in Biomedicine, Department of Human Pathology, IM Sechenov First Moscow State Medical University, Russian Federation.
Hülya BayırDepartment of Critical Care Medicine, Safar Center for Resuscitation Research, Children's Hospital of Pittsburgh, Pittsburgh, PA, USA; Department of Environmental and Occupational Health, Center for Free Radical and Antioxidant Health, University of Pittsburgh, Pittsburgh, PA, USA; Children's Neuroscience Institute, UPMC Children's Hospital of Pittsburgh, Pittsburgh, PA, USA. Electronic address: bayihx@ccm.upmc.edu.

Funding

Training and EducationU19AI068021 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GREENBERGER, JOEL S · 2005 to 2019
$44.4M
Regulation of Cardiolin Byosynthesis in Epithelial InjuryP01HL114453 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI MALLAMPALLI, RAMA K · 2014 to 2023
$21.3M
Mapping Lipid Oxidation in Traumatic Brain Injury by Mass Spectrometric ImagingR01NS076511 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Hülya Bayir, Valerian E Kagan · 2012 to 2026
$6.8M
Oxidative Lipidomics in Pediatric Traumatic Brain InjuryR01NS061817 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BAYIR, HÜLYA · 2008 to 2018
$3.3M
Oxidative Lipidomics in Pediatric Traumatic Brain InjuryR37NS061817 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Hülya Bayir · 2021 to 2026
$2.2M
Mitochondria-Targeted Redox Therapy for Cerebral Ischemia in the Developing BrainR01NS084604 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BAYIR, HÜLYA, CLARK, ROBERT S B · 2014 to 2018
$2.0M
NHLBI NIH HHS P01 HL114453NIAID NIH HHS U19 AI068021NINDS NIH HHS R01 NS061817NINDS NIH HHS R01 NS076511NINDS NIH HHS R01 NS084604NINDS NIH HHS R37 NS061817
6 · The paper itself

Abstract

Mitochondria are a keystone of neuronal function, serving a dual role as sustainer of life and harbinger of death. While mitochondria are indispensable for energy production, a dysregulated mitochondrial network can spell doom for both neurons and the functions they provide. Traumatic brain injury (TBI) is a complex and biphasic injury, often affecting children and young adults. The primary pathological mechanism of TBI is mechanical, too rapid to be mitigated by anything but prevention. However, the secondary injury of TBI evolves over hours and days after the initial insult providing a window of opportunity for intervention. As a nexus point of both survival and death during this second phase, targeting mitochondrial pathology in TBI has long been an attractive strategy. Often these attempts are mired by efficacy-limiting unintended off-target effects. Specific delivery to and enrichment of therapeutics at their submitochondrial site of action can reduce deleterious effects and increase potency. Mitochondrial drug localization is accomplished using (1) the mitochondrial membrane potential, (2) affinity of a carrier to mitochondria-specific components (e.g. lipids), (3) piggybacking on the cells own mitochondria trafficking systems, or (4) nanoparticle-based approaches. In this review, we briefly consider the mitochondrial delivery strategies and drug targets that illustrate the promise of these mitochondria-specific approaches in the design of TBI pharmacotherapy. This article is part of the Special Issue entitled "Novel Treatments for Traumatic Brain Injury".

Indexed as

AnimalsBrain Injuries, TraumaticCentral Nervous System AgentsHumansMitochondriaCentral Nervous System AgentsDrug developmentDrug discoveryMitochondriaMitochondria-localizing drugTraumatic brain injury

Identifiers

PMID30009835
PMCPMC6309489

What OpenQuestion holds

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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.