Evidence map›Paper›PMID 42828096›Full record

ArticleMaterials today. Bio2026

An FGF21-based fusion protein ameliorates mitochondrial dysfunction and promotes recovery post spinal cord injury.

Xuehai Chen, Yibo Ying, Yuchao Zhang, Jiali Lv, Minghao Jiang, Yujun Mo, Zhiyi Wu, Huixin Lin, Zhiyang Huang, Dawei Jiang and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Materials today. Bio, 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

13 authors.

Xuehai ChenDepartment of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Yibo YingDepartment of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Yuchao ZhangDepartment of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Jiali LvDepartment of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Minghao JiangDepartment of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Yujun MoDepartment of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Zhiyi WuDepartment of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Huixin LinDepartment of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Zhiyang HuangDepartment of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Dawei JiangDepartment of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Yanming ZuoDepartment of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Xiaokun LiDepartment of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Zhouguang WangDepartment of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial dysfunction and defective repair are central drivers of secondary injury following spinal cord injury (SCI), yet effective strategies to restore mitochondrial quality control remain limited. Here, we develop an engineered long-acting fibroblast growth factor 21 fusion protein (SFGF21) by incorporating a linker peptide to enhance molecular targeting and oxidative stability. In a mouse model of SCI, sustained delivery of SFGF21 specifically potentiated dynamic crosstalk between mitochondria and lysosomes, thereby activating the BNIP3/BNIP3L pathway-mediated mitophagic flux and clearing dysfunctional mitochondria in injured neurons. This process restored mitochondrial homeostasis, suppressed lipid peroxidation, and alleviated oxidative stress in injured neurons. Loss-of-function experiments confirmed that both FGFR1 and BNIP3 are required for SFGF21-induced mitophagy and neuroprotection. Together, our findings establish engineered modulation of organelle crosstalk as a therapeutic strategy to activate mitophagy and support neural repair after SCI, highlighting mitochondria-targeted protein engineering as a potential therapeutic path for spinal cord repair.

Indexed as

FerroptosisMitochondria–lysosome crosstalkMitophagySFGF21Spinal cord injury

Identifiers

PMID42828096
PMCPMC13631618

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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.