Evidence map›Paper›PMID 42109613›Full record

ArticleBurns & trauma2026

Targeting mitofusin 1-mediated mitochondrial dynamics to suppress neuroinflammation and pyroptosis after traumatic brain injury.

Tao Liu, Liang Mi, Bo Chen, Meng Nie, Shuo Wang, Bo Wang, Yunhu Yu, Rongcai Jiang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

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

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

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.

Tao LiuDepartment of Neurosurgery, Xuanwu Hospital, Capital Medical University, 45 Changchun Street, Xicheng District, Beijing 100053, China.ORCID https://orcid.org/0000-0002-0506-3356
Liang MiDepartment of Neurosurgery, Tianjin Neurological Institute, State Key Laboratory of Experimental Hematology, Laboratory of Post-Neuroinjury Neurorepair and Regeneration in Central Nervous System Tianjin and Ministry of Education, Tianjin Medical University General Hospital, 154 Anshan Road, Heping District, Tianjin 300052, China.
Bo ChenDepartment of Neurosurgery, Xuanwu Hospital, Capital Medical University, 45 Changchun Street, Xicheng District, Beijing 100053, China.
Meng NieDepartment of Neurosurgery, Tianjin Neurological Institute, State Key Laboratory of Experimental Hematology, Laboratory of Post-Neuroinjury Neurorepair and Regeneration in Central Nervous System Tianjin and Ministry of Education, Tianjin Medical University General Hospital, 154 Anshan Road, Heping District, Tianjin 300052, China.
Shuo WangDepartment of Neurosurgery, Tianjin Neurological Institute, State Key Laboratory of Experimental Hematology, Laboratory of Post-Neuroinjury Neurorepair and Regeneration in Central Nervous System Tianjin and Ministry of Education, Tianjin Medical University General Hospital, 154 Anshan Road, Heping District, Tianjin 300052, China.
Bo WangDepartment of Neurosurgery, Tianjin Neurological Institute, State Key Laboratory of Experimental Hematology, Laboratory of Post-Neuroinjury Neurorepair and Regeneration in Central Nervous System Tianjin and Ministry of Education, Tianjin Medical University General Hospital, 154 Anshan Road, Heping District, Tianjin 300052, China.
Yunhu YuDepartment of Neurosurgery, The People's Hospital of Hong Hua Gang District of Zun Yi, No. 185, Wanli Road, Honghuagang District, Zunyi 563000, Guizhou, China.
Rongcai JiangDepartment of Neurosurgery, Xuanwu Hospital, Capital Medical University, 45 Changchun Street, Xicheng District, Beijing 100053, China.ORCID https://orcid.org/0009-0002-0851-3786

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Traumatic brain injury (TBI) can cause neuroinflammation and neuronal death. The role of mitochondrial dysfunction in regulating inflammasome activation during TBI remains unclear. This study aims to explore mitochondrial regulation of neuroinflammation and pyroptosis after TBI. Methods: We used a mouse TBI model and Results: TBI triggered NLRP3 inflammasome activation and neuronal pyroptosis, along with impaired mitochondrial function and oxidative stress. Metformin reduced inflammasome activation, improved mitochondrial homeostasis, and alleviated neuronal injury. These effects were lost when Mfn1 was silenced, highlighting its essential role. Furthermore, we determined that the AMPK pathway modulates these observed effects. Conclusion: Metformin protects against TBI-induced neuronal damage by restoring Mfn1-dependent mitochondrial dynamics and suppressing inflammasome activation. Mfn1 is a key mediator linking mitochondrial health to neuroinflammatory responses in TBI.

Indexed as

MetforminMitochondrial dynamicsMitofusin 1NLRP3 inflammasomePyroptosisTraumatic brain injury

Identifiers

PMID42109613
PMCPMC13152094

What Socratic holds

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LicenceCC BY
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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 Socratic graph.