Evidence map›Paper›PMID 41914681›Full record

ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2026

Cross-species evidence for cardiolipin remodeling in neonatal hypoxic-ischemic encephalopathy.

Katlynn J Emaus, Garrett M Fogo, Sarita Raghunayakula, Erin Gruley, Liam McCracken, Caroline Dubs, Reagan L Speas, Francisco J Torres Torres, Joseph M Wider, Thomas H Sanderson

Abstract read
In one paragraph

Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

10 authors.

Katlynn J EmausNeuroscience Graduate Program, University of Michigan, Ann Arbor, MI, USA.ORCID 0000-0003-2136-6450
Garrett M FogoNeuroscience Graduate Program, University of Michigan, Ann Arbor, MI, USA.
Sarita RaghunayakulaDepartment of Emergency Medicine, University of Michigan, Ann Arbor, MI, USA.
Erin GruleyDepartment of Emergency Medicine, University of Michigan, Ann Arbor, MI, USA.
Liam McCrackenDepartment of Emergency Medicine, University of Michigan, Ann Arbor, MI, USA.
Caroline DubsDepartment of Emergency Medicine, University of Michigan, Ann Arbor, MI, USA.
Reagan L SpeasNeuroscience Graduate Program, University of Michigan, Ann Arbor, MI, USA.
Francisco J Torres TorresNeuroscience Graduate Program, University of Michigan, Ann Arbor, MI, USA.
Joseph M WiderNeuroscience Graduate Program, University of Michigan, Ann Arbor, MI, USA.
Thomas H SandersonNeuroscience Graduate Program, University of Michigan, Ann Arbor, MI, USA.ORCID 0000-0003-0112-8164

Funding

Training Program in Perinatal Biology and MedicineT32HD007186 · NICHD · UNIVERSITY OF COLORADO DENVER · PI Paul Joseph Rozance · 1985 to 2026
$6.5M
Development and Testing of LUCID: A Therapeutic Device for Brain Injury Following Infant Cardiac ArrestU44NS125160 · NINDS · MITOVATION, INC. · PI MAIK HUETTEMANN, Thomas Hudson Sanderson · 2022 to 2026
$3.6M
Non-invasive mitochondrial modulation therapy for ischemic strokeR01NS120322 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HUETTEMANN, MAIK, SANDERSON, THOMAS HUDSON · 2021 to 2025
$2.3M
Training Program in Translational Cardiovascular Research and EntrepreneurshipT32HL125242 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MICHELE, DANIEL E · 2015 to 2024
$1.9M
Infant NeuroLUX: A Novel Non-invasive Therapeutic Device for Neonatal Hypoxic Brain InjuryR42NS105238 · NINDS · MITOVATION, INC. · PI HUETTEMANN, MAIK, SANDERSON, THOMAS HUDSON · 2018 to 2020
$1.8M
Evaluation of Mitochondrial Cardiolipin Modification in Neonatal Hypoxia/Ischemia EncephalopathyF31NS129326 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI EMAUS, KATLYNN JOY · 2023 to 2025
$101k
NHLBI NIH HHS T32 HL125242NICHD NIH HHS T32 HD007186NINDS NIH HHS F31 NS129326NINDS NIH HHS R01 NS120322NINDS NIH HHS R42 NS105238NINDS NIH HHS U44 NS125160
6 · The paper itself

Abstract

Neonatal hypoxic-ischemic encephalopathy (HIE) is a leading cause of infant mortality and long-term neurological disability. Current treatments offer limited efficacy, especially in premature or severely affected infants. The pathology of HIE involves a cascade of cellular damage initiated by oxygen and nutrient deprivation, followed by reperfusion injury characterized by excessive reactive oxygen species (ROS) production and mitochondrial dysfunction. Cardiolipin (CL), a mitochondria-specific phospholipid, plays a critical role in maintaining mitochondrial integrity, dynamics, and quality control through mitophagy and programmed cell death. In this study, we examined changes in CL subspecies in an in vitro ischemia/reperfusion model and small and large animal models of neonatal HIE. We observed a significant increase in the ratio of monolysocardiolipin (MLCL) to CL and significant increase in saturated CL species following injury. Genetic ablation of Tafazzin protein using conditional

Indexed as

CardiolipinsHypoxia-Ischemia, BrainAnimalsAnimals, NewbornDisease Models, AnimalLysophospholipidsMiceMice, KnockoutMitochondriaReactive Oxygen SpeciesReperfusion InjuryTranscription FactorsCardiolipinsLysophospholipidsmonolysocardiolipinReactive Oxygen SpeciesTranscription FactorsAnimal modelscardiolipinischemia–reperfusion injurymitochondrial dysfunctionneonatal hypoxia–ischemia encephalopathy

Identifiers

PMID41914681
PMCPMC13038497

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.