Evidence map›Paper›PMID 38539837›Full record

ReviewAntioxidants (Basel, Switzerland)2024

Mitochondria-Targeted Antioxidant Therapeutics for Traumatic Brain Injury.

Hiren R Modi, Sudeep Musyaju, Meaghan Ratcliffe, Deborah A Shear, Anke H Scultetus, Jignesh D Pandya

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

Review in Antioxidants (Basel, Switzerland), 2024. 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
9.2field-weighted citation impact, top 1% 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, 25 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Hiren R ModiBrain Trauma Neuroprotection (BTN) Branch, Center for Military Psychiatry and Neuroscience, Walter Reed Army Institute of Research (WRAIR), 503 Robert Grant Avenue, Silver Spring, MD 20910, USA.
Sudeep MusyajuBrain Trauma Neuroprotection (BTN) Branch, Center for Military Psychiatry and Neuroscience, Walter Reed Army Institute of Research (WRAIR), 503 Robert Grant Avenue, Silver Spring, MD 20910, USA.
Meaghan RatcliffeBrain Trauma Neuroprotection (BTN) Branch, Center for Military Psychiatry and Neuroscience, Walter Reed Army Institute of Research (WRAIR), 503 Robert Grant Avenue, Silver Spring, MD 20910, USA.
Deborah A ShearBrain Trauma Neuroprotection (BTN) Branch, Center for Military Psychiatry and Neuroscience, Walter Reed Army Institute of Research (WRAIR), 503 Robert Grant Avenue, Silver Spring, MD 20910, USA.
Anke H ScultetusBrain Trauma Neuroprotection (BTN) Branch, Center for Military Psychiatry and Neuroscience, Walter Reed Army Institute of Research (WRAIR), 503 Robert Grant Avenue, Silver Spring, MD 20910, USA.
Jignesh D PandyaBrain Trauma Neuroprotection (BTN) Branch, Center for Military Psychiatry and Neuroscience, Walter Reed Army Institute of Research (WRAIR), 503 Robert Grant Avenue, Silver Spring, MD 20910, USA.ORCID 0000-0003-3281-5792
Walter Reed Army Institute of Research · US

Funding

Combat Casualty Care Research Program CO240012_WRAIR (FY24-26)Combat Casualty Care Research Program H_001_2018_WRAIR (FY18-23)
6 · The paper itself

Abstract

Traumatic brain injury (TBI) is a major global health problem that affects both civilian and military populations worldwide. Post-injury acute, sub-acute, and chronic progression of secondary injury processes may contribute further to other neurodegenerative diseases. However, there are no approved therapeutic options available that can attenuate TBI-related progressive pathophysiology. Recent advances in preclinical research have identified that mitochondria-centric redox imbalance, bioenergetics failure and calcium dysregulation play a crucial role in secondary injury progression after TBI. Mitochondrial antioxidants play an important role in regulating redox homeostasis. Based on the proven efficacy of preclinical and clinical compounds and targeting numerous pathways to trigger innate antioxidant defense, we may be able to alleviate TBI pathology progression by primarily focusing on preserving post-injury mitochondrial and cerebral function. In this review, we will discuss novel mitochondria-targeted antioxidant compounds, which offer a high capability of successful clinical translation for TBI management in the near future.

Indexed as

antioxidantscell deathfree radicalsmitochondrianeuroprotectionoxidative stresstherapeuticstraumatic brain injury

Identifiers

PMID38539837
PMCPMC10967339
OpenAlexW4394762329

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.