Evidence map›Paper›PMID 41068806›Full record

ArticleJournal of nanobiotechnology2025

Bispecific self-assembled peptides as supra-growth factors for preventing endotheliopathy and improving survival of traumatic brain injury in mice.

Yichi Zhang, Lanxing Wang, Dandan Li, Xingyao Sun, Zijian Zhou, Ying Zhang, Linan Jiao, Shuhong Yang, Yafan Liu, Tianrui Ma and 10 more

Abstract read
In one paragraph

Article in Journal of nanobiotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

20 authors.

Yichi Zhang *Tianjin Institute of Neurology, Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Lanxing Wang *State Key Laboratory of Medicinal Chemical Biology and College of Life Sciences, Nankai University, Tianjin, 300071, China.
Dandan Li *State Key Laboratory of Medicinal Chemical Biology and College of Life Sciences, Nankai University, Tianjin, 300071, China.
Xingyao SunState Key Laboratory of Medicinal Chemical Biology and College of Life Sciences, Nankai University, Tianjin, 300071, China.
Zijian ZhouTianjin Institute of Neurology, Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Ying ZhangState Key Laboratory of Medicinal Chemical Biology and College of Life Sciences, Nankai University, Tianjin, 300071, China.
Linan JiaoTianjin Institute of Neurology, Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Shuhong YangTianjin Institute of Neurology, Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Yafan LiuTianjin Institute of Neurology, Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Tianrui MaTianjin Institute of Neurology, Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Hao ZhangTianjin Institute of Neurology, Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Lujia TangTianjin Institute of Neurology, Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Kaifeng PangTianjin Institute of Neurology, Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Pengbo ZhaoTianjin Institute of Neurology, Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Muyan XuTianjin Institute of Neurology, Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Jie LiState Key Laboratory of Medicinal Chemical Biology and College of Life Sciences, Nankai University, Tianjin, 300071, China.
Jianning ZhangTianjin Institute of Neurology, Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Zhimou YangNankai International Advanced Research Institute (Shenzhen Futian), Nankai University, Shenzhen, 518045, Guangdong, P. R. China.
Jie GaoState Key Laboratory of Medicinal Chemical Biology and College of Life Sciences, Nankai University, Tianjin, 300071, China. chemgaojie@nankai.edu.cn.
Zilong ZhaoTianjin Institute of Neurology, Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin, 300052, China. zilongzhaotianjin@hotmail.com.

Funding

National Natural Science Foundation of China 32201094National Natural Science Foundation of China 82022020National Natural Science Foundation of China T2122019Science and Technology Planning Projects of Tianjin Municipality 24ZXZSSS00030Shenzhen Science and Technology Program KQTD20240729102037042Tianjin Natural Science Foundation 23JCZXJC00330
6 · The paper itself

Abstract

Traumatic brain injury (TBI) causes endothelial injury (endotheliopathy), which contributes to a cascade of adverse events, including cerebral hemorrhage, edema and acute lung injury (ALI), and leads to poor clinical outcomes. Protecting endothelial integrity and targeting cerebral endothelium is therefore critical for preventing secondary cerebral injuries from TBI. However, effective treatment strategies in the clinic remain lacking. Here, we report a nanofiber of bispecific self-assembled peptide (BsSA) as a supra-growth factor that possesses multiple functions, such as binding to the blood‒brain barrier (BBB) and dual growth factor activity. BsSA protects TBI mice by binding to the BBB through Insulin-like growth factor 1 receptor (IGF-1R) and insulin receptor (IR) and ameliorating endothelial injury by activating the IGF-1R/IR signaling pathway. Specifically, this protection is achieved by promoting endothelial cell proliferation and survival and mitigating oxidative stress. Exogenous BsSA, as a therapeutic agent, prevented mice with TBI from developing brain and pulmonary endotheliopathy and improved their outcomes. This study identified BsSA as a potential therapeutic agent to reduce TBI-induced endotheliopathy, brain edema, and lung injury and improve TBI outcomes.

Indexed as

Brain Injuries, TraumaticPeptidesAnimalsBlood-Brain BarrierBrain EdemaCell ProliferationDisease Models, AnimalEndothelial CellsHumansMaleMiceMice, Inbred C57BLOxidative StressReceptor, IGF Type 1Receptor, InsulinSignal TransductionPeptidesReceptor, IGF Type 1Receptor, InsulinDrug deliveryEndotheliopathyNanoscale materialsSelf-assembled peptidesTraumatic brain injury

Identifiers

PMID41068806
PMCPMC12512954

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.