Evidence map›Paper›PMID 24201802›Full record

ArticleCell death & disease2013

Nanoparticle-mediated catalase delivery protects human neurons from oxidative stress.

A Singhal, V B Morris, V Labhasetwar, A Ghorpade

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
3.2field-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

75 citing papers in PubMed, 158 citations in OpenAlex.

  1. Article
  2. Mitochondria-targeted delivery strategies for age-related diseases.International journal of pharmaceutics: X · 2026
    Review
  3. Article
  4. Review
  5. Article
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  7. Article
  8. Review
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  10. Article
  11. Review
  12. Review
  13. Article
  14. Effects of Heat-Induced Oxidative Stress and Astaxanthin on theCurrent issues in molecular biology · 2024
    Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Catalytic antioxidant nanoparticles mitigate secondary injury progression and promote functional recovery in spinal cord injury model.Journal of controlled release : official journal of the Controlled Release Society · 2023
    Article

15 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

A SinghalDepartment of Cell Biology and Anatomy, University of North Texas Health Science Center, Fort Worth, TX, USA.
V B Morris
V Labhasetwar
A Ghorpade
Cleveland Clinic Lerner College of Medicine · USUniversity of North Texas · USUniversity of North Texas Health Science Center · US

Funding

LABORATORY OF DEVELOPMENTAL BIOLOGYR24HD000836 · NICHD · UNIVERSITY OF WASHINGTON · PI Ian Amos Glass · 1995 to 2026
$16.9M
Neuronal Survival, HIV-1 and Astrocyte-TIMP-1R01NS048837 · NINDS · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI BORGMANN, KATHLEEN · 2005 to 2018
$5.2M
Stroke TherapyR01NS070896 · NINDS · CLEVELAND CLINIC LERNER COM-CWRU · PI LABHASETWAR, VINOD D · 2010 to 2014
$2.3M
Pineal Regulation: Control of arylalkylamine N-acetyltransferaseZ01HD008836 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI KLEIN, DAVID · 2007 to 2008
$2.0M
Intramural NIH HHS Z01 HD008836NICHD NIH HHS 5R24HD0008836NICHD NIH HHS R24 HD000836NINDS NIH HHS R01 NS048837NINDS NIH HHS R01 NS070896NINDS NIH HHS R01 NS070896-01NINDS NIH HHS R01 NS48837
6 · The paper itself

Abstract

Several neurodegenerative diseases and brain injury involve reactive oxygen species and implicate oxidative stress in disease mechanisms. Hydrogen peroxide (H2O2) formation due to mitochondrial superoxide leakage perpetuates oxidative stress in neuronal injury. Catalase, an H2O2-degrading enzyme, thus remains an important antioxidant therapy target. However, catalase therapy is restricted by its labile nature and inadequate delivery. Here, a nanotechnology approach was evaluated using catalase-loaded, poly(lactic co-glycolic acid) nanoparticles (NPs) in human neuronal protection against oxidative damage. This study showed highly efficient catalase encapsulation capable of retaining ~99% enzymatic activity. NPs released catalase rapidly, and antioxidant activity was sustained for over a month. NP uptake in human neurons was rapid and nontoxic. Although human neurons were highly sensitive to H2O2, NP-mediated catalase delivery successfully protected cultured neurons from H2O2-induced oxidative stress. Catalase-loaded NPs significantly reduced H2O2-induced protein oxidation, DNA damage, mitochondrial membrane transition pore opening and loss of cell membrane integrity and restored neuronal morphology, neurite network and microtubule-associated protein-2 levels. Further, catalase-loaded NPs improved neuronal recovery from H2O2 pre-exposure better than free catalase, suggesting possible applications in ameliorating stroke-relevant oxidative stress. Brain targeting of catalase-loaded NPs may find wide therapeutic applications for oxidative stress-associated acute and chronic neurodegenerative disorders.

Indexed as

CatalaseCells, CulturedHumansHydrogen PeroxideLactic AcidNanoparticlesNeuronsOxidative StressPolyglycolic AcidPolylactic Acid-Polyglycolic Acid CopolymerCatalaseHydrogen PeroxideLactic AcidPolyglycolic AcidPolylactic Acid-Polyglycolic Acid Copolymer

Identifiers

PMID24201802
PMCPMC3847304
OpenAlexW2075200744

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.