Evidence map›Paper›PMID 40320408›Full record

ArticleScientific reports2025

Irisin suppressed the progression of TBI via modulating AMPK/MerTK/autophagy and SYK/ROS/inflammatory signaling.

Kuo Zhang, Yihui Du, Sihui Yang, Guozhu Sun

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Kuo ZhangDepartment of Neurosurgery, The Second Hospital of Hebei Medical University, Shijiazhuang City, 050000, Hebei Province, China.
Yihui DuDepartment of Neurosurgery, Hebei General Hospital, Shijiazhuang City, 050000, Hebei Province, China.
Sihui YangDepartment of Neurosurgery, Hebei General Hospital, Shijiazhuang City, 050000, Hebei Province, China.
Guozhu SunDepartment of Neurosurgery, The Second Hospital of Hebei Medical University, Shijiazhuang City, 050000, Hebei Province, China. Sungzh705@hebmu.edu.cn.

Funding

the Government-funded Provincial Medical Talent Project of China Grant No. 303-2022-27-02the Hebei Provincial Natural Science Foundation of China Grant No.H2020206437the Key Medical Scientific Research Project of Hebei Province of China Grant no. 20220112;20230032This research was supported by the S&T Program of Hebei Grant No.22377717D
6 · The paper itself

Abstract

Irisin is a hormone-like peptide secreted by muscle tissues and generated by hydrolysis of type III fibronectin domain-containing protein 5 by proteolytic hydrolases. Whether Irisin has a potential protective role in traumatic brain injury (TBI). In this study, we will investigate the relevant research progress of Irisin's protective role in traumatic brain injury (TBI) in recent years in terms of attenuating oxidative stress, inhibiting pyroptosis, suppressing inflammatory response, and improving autophagy, with the aim of providing valuable references for the diagnosis and treatment of traumatic brain injury (TBI). Utilize bioinformatics analysis to study the interactions between genes in TBI (Traumatic Brain Injury). Construct a TBI mouse model to observe the effects of Irisin on TBI. The Morris water maze test is used to assess the learning and spatial memory abilities of mice, TUNEL fluorescence is used to detect cell apoptosis, Nissl staining is employed to observe the survival of hippocampal neurons in mice, and HE staining is used to observe the extent of brain injury in mice. Western blot is used to detect protein expression in both in vivo and in vitro experiments. Q-PCR is employed to detect the levels of proteins related to autophagy/pyroptosis/inflammation. Irisin promotes MerTK overexpression by enhancing AMPK activation. Irisin can increase the expression of LC3I and Beclin-1 proteins, indicating the promotion of autophagic response. Additionally, Irisin reduces ROS levels and decreases SYK expression, thereby inhibiting the inflammatory response. Irisin improves the learning and spatial memory abilities of TBI mice and reduces cell apoptosis, as well as decreases hippocampal neuron death. HE staining shows that the brain injury in mice treated with Irisin is significantly alleviated. Irisin can enhance the expression of phosphorylated AMPK and phosphorylated MerTK proteins, promote autophagic response, and inhibit pyroptosis/inflammatory response. Correction experiments confirmed that after stimulation with an AMPK agonist, the expression of phosphorylated MerTK protein is significantly increased, autophagic response is enhanced, and pyroptosis/inflammatory response is weakened. When treated with a MerTK inhibitor during AMPK agonist stimulation, the autophagic response is weakened while pyroptosis/inflammatory response is enhanced. Irisin can inhibit the progression of traumatic brain injury by regulating AMPK/MerTK/autophagy and SYK/ROS/inflammatory signaling.

Indexed as

AMP-Activated Protein KinasesAutophagyBrain Injuries, TraumaticFibronectinsAnimalsApoptosisDisease Models, AnimalHippocampusInflammationMaleMiceMice, Inbred C57BLNeuronsReactive Oxygen SpeciesSignal TransductionSyk KinaseAMP-Activated Protein KinasesFibronectinsFNDC5 protein, mouseReactive Oxygen SpeciesSyk KinaseSyk protein, mouseAMPK/MerTKAutophagyFocal deathIrisinSYK/ROSTraumatic brain injury (TBI)

Identifiers

PMID40320408
PMCPMC12050266

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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.