Evidence map›Paper›PMID 41796420›Full record

ArticleTranslational stroke research2026

Remote Ischemic Preconditioning Exerts Neuroprotective Effects Via the PGC-1α/FNDC5/BDNF Pathway in Focal Brain Ischemia of Rats.

Teruki Matsuoka, Ryoma Matsuzaki, Kazuki Nakanishi, Shogo Kakimoto, Yuki Kato, Shotaro Otsuka, Kiyoshi Kikuchi, Harutoshi Sakakima

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Article in Translational stroke research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

8 authors.

Teruki MatsuokaDepartment of Physical Therapy, School of Health Sciences, Faculty of Medicine, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8544, Japan.
Ryoma MatsuzakiDepartment of Physical Therapy, School of Health Sciences, Faculty of Medicine, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8544, Japan.
Kazuki NakanishiDepartment of Physical Therapy, School of Health Sciences, Faculty of Medicine, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8544, Japan.
Shogo KakimotoDepartment of Physical Therapy, School of Health Sciences, Faculty of Medicine, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8544, Japan.
Yuki KatoDepartment of Physical Therapy, School of Health Sciences, Faculty of Medicine, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8544, Japan.
Shotaro OtsukaFaculty of Welfare and Health Science, Oita University, Oita, Japan.
Kiyoshi KikuchiDivision of Brain Science, Department of Physiology, Kurume University School of Medicine, Kurume, Japan.
Harutoshi SakakimaDepartment of Physical Therapy, School of Health Sciences, Faculty of Medicine, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8544, Japan. sakaki@health.nop.kagoshima-u.ac.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Remote ischemic preconditioning (RIpreC) is a strategy for remotely protecting target organs such as the brain by applying brief ischemia and reperfusion to the limb. However, the mechanisms underlying RIpreC-induced neuroprotection remain unclear. We aimed to investigate the neuroprotective effects of RIpreC on the peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (PGC-1α)/ fibronectin type III domain-containing protein 5 (FNDC5)/ brain-derived neurotrophic factor (BDNF) pathway in rat models of ischemic stroke. Rats were assigned to three groups: ischemia-reperfusion injury (IR, n = 11), RIpreC and IR (RIpreC, n = 11), and intact control (control, n = 5). RIpreC was performed approximately 24 h before IR injury. IR injury induced by middle cerebral artery occlusion (MCAO) for 60 min. At 2 days after MCAO, brain infarction, sensorimotor functions, and the expression of PGC-1α, FNDC5/irisin, BDNF, B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), caspase-3, terminal deoxynucleotidyl transferase-mediated biotinylated dUTP nick end labeling (TUNEL)-positive cells, and the p-Akt/Akt ratio were examined. In addition, SR-18,292, a PGC-1α inhibitor, was administered 1 h before MCAO. The RIpreC group had a significantly reduced infarct volume and ameliorated sensorimotor function compared with the IR group. RIpreC increased the expression of PGC-1α, FNDC5, BDNF, and the p-Akt/Akt ratio in the ischemic brain. Bax/Bcl-2 ratios, as well as perilesional caspase-3- and TUNEL-positive neuronal cells, decreased following RIpreC. Inhibition of PGC-1α blunted the RIpreC-induced neuroprotective and neurorestorative effects. This study suggests that RIpreC induced BDNF expression through a PGC-1α/FNDC5 pathway after ischemic stroke, thereby exerting neuroprotection and ameliorating post-stroke neurobehavioral dysfunctions.

Indexed as

Brain-Derived Neurotrophic FactorBrain IschemiaFibronectinsIschemic PreconditioningPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaAnimalsDisease Models, AnimalInfarction, Middle Cerebral ArteryMaleRatsRats, Sprague-DawleyReperfusion InjurySignal TransductionBdnf protein, ratBrain-Derived Neurotrophic FactorFibronectinsFNDC5 protein, ratPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, ratBDNFIrisinIschemic strokeNeuroprotectionPGC-1αRIpreC

Identifiers

PMID41796420
PMCPMC12968114

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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.