Evidence map›Paper›PMID 25613139›Full record

ArticleCurrent HIV research2014

Creatine protects against mitochondrial dysfunction associated with HIV-1 Tat-induced neuronal injury.

Patrick R Stevens, Jeremy W Gawryluk, Liang Hui, Xuesong Chen, Jonathan D Geiger

Abstract read
In one paragraph

Article in Current HIV research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

18 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Inhibition of the Dead Box RNA Helicase 3 Prevents HIV-1 Tat and Cocaine-Induced Neurotoxicity by Targeting Microglia Activation.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2020
    Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Metabolomic Responses to Manganese Dose in SH-SY5Y Human Neuroblastoma Cells.Toxicological sciences : an official journal of the Society of Toxicology · 2019
    Article
  9. Article
  10. Targeted Mitochondrial COQMolecular pharmaceutics · 2019
    Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. HIV-1 Tat and Cocaine Impair Survival of Cultured Primary Neuronal Cells via a Mitochondrial Pathway.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2016
    Article
  18. Review
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

5 authors at 1 institution in 1 country.

Patrick R Stevens
Jeremy W Gawryluk
Liang Hui
Xuesong Chen
Jonathan D GeigerDepartment of Basic Biomedical Sciences, University of North Dakota School of Medicine and Health Sciences, 504 Hamline St., Grand Forks, North Dakota 58203, USA. jonathan.geiger@med.und.edu.
University of North Dakota · US

Funding

Pilot Projects CoreP30GM103329 · NIGMS · UNIVERSITY OF NORTH DAKOTA · PI GEIGER, JONATHAN DAVID · 2012 to 2016
$5.1M
The Role of Adenosine in Ketogenic Diet TherapyR01NS065957 · NINDS · TRINITY COLLEGE · PI BOISON, DETLEV, GEIGER, JONATHAN DAVID · 2010 to 2021
$3.9M
The role of novel endolysosome-dependent calcium regulatory mechanisms in HIV-1 TR01MH100972 · NIMH · UNIVERSITY OF NORTH DAKOTA · PI CHEN, XUESONG, GEIGER, JONATHAN DAVID · 2014 to 2018
$1.6M
Neuronal endolysosome involvement in HIV-1 Tat-induced amyloid beta accumulationR21AG043338 · NIA · UNIVERSITY OF NORTH DAKOTA · PI CHEN, XUESONG, GEIGER, JONATHAN DAVID · 2012 to 2013
$336k
NIA NIH HHS R21 AG043338NIA NIH HHS R21AG043338NIGMS NIH HHS P30 GM103329NIGMS NIH HHS P30GM103329NIMH NIH HHS R01 MH100972NIMH NIH HHS R01MH100972NINDS NIH HHS R01 NS065957
6 · The paper itself

Abstract

HIV-1 infected individuals live longer but experience a prevalence rate of over 50% for HIV-1 associated neurocognitive disorders (HAND) for which no effective treatment is available. Viral and cellular factors secreted by HIV-1 infected cells lead to neuronal injury and HIV-1 Tat continues to be implicated in the pathogenesis of HAND. Here we tested the hypothesis that creatine protected against HIV-1 Tat-induced neuronal injury by preventing mitochondrial bioenergetic crisis and/or redox catastrophe. Creatine blocked HIV-1 Tat(1-72)-induced increases in neuron cell death and synaptic area loss. Creatine protected against HIV-1 Tat-induced decreases in ATP. Creatine and creatine plus HIV-1 Tat increased cellular levels of creatine, and creatine plus HIV-1 Tat further decreased ratios of phosphocreatine to creatine observed with creatine or HIV-1 Tat treatments alone. Additionally, creatine protected against HIV-1 Tat-induced mitochondrial hypopolarization and HIV-1 Tat-induced mitochondrial permeability transition pore opening. Thus, creatine may be a useful adjunctive therapy against HAND.

Indexed as

AnimalsCell DeathCells, CulturedCreatineFemaleHIV-1Metabolic Networks and PathwaysMice, Inbred C57BLMitochondriaNeuronsNeuroprotective AgentsOxidation-Reductiontat Gene Products, Human Immunodeficiency VirusCreatineNeuroprotective Agentstat Gene Products, Human Immunodeficiency Virus

Identifiers

PMID25613139
PMCPMC4372859
OpenAlexW2111613263

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.