Evidence map›Paper›PMID 40857429›Full record

ArticleAdvanced functional materials2025

Functional hydrogel for modulating lipid droplets and neuroinflammation in head injury.

Feixiang Chen, Yvonne Shen, Yutong Shao, Tenghuan Ge, Haowen Qiao, Shangzhou Xia, Yafei Qu, Yuanpu Chiu, Ying Qin, Zhen Zhao

Abstract read
In one paragraph

Article in Advanced functional materials, 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

10 authors.

Feixiang ChenCenter for Neurodegeneration and Regeneration, Zilkha Neurogenetic Institute, Department of Physiology and Biophysics, Keck School of Medicine, University of Southern California, Los Angeles, California, 90033, USA.
Yvonne ShenCenter for Neurodegeneration and Regeneration, Zilkha Neurogenetic Institute, Department of Physiology and Biophysics, Keck School of Medicine, University of Southern California, Los Angeles, California, 90033, USA.
Yutong ShaoCenter for Neurodegeneration and Regeneration, Zilkha Neurogenetic Institute, Department of Physiology and Biophysics, Keck School of Medicine, University of Southern California, Los Angeles, California, 90033, USA.
Tenghuan GeCenter for Neurodegeneration and Regeneration, Zilkha Neurogenetic Institute, Department of Physiology and Biophysics, Keck School of Medicine, University of Southern California, Los Angeles, California, 90033, USA.
Haowen QiaoCenter for Neurodegeneration and Regeneration, Zilkha Neurogenetic Institute, Department of Physiology and Biophysics, Keck School of Medicine, University of Southern California, Los Angeles, California, 90033, USA.
Shangzhou XiaCenter for Neurodegeneration and Regeneration, Zilkha Neurogenetic Institute, Department of Physiology and Biophysics, Keck School of Medicine, University of Southern California, Los Angeles, California, 90033, USA.
Yafei QuCenter for Neurodegeneration and Regeneration, Zilkha Neurogenetic Institute, Department of Physiology and Biophysics, Keck School of Medicine, University of Southern California, Los Angeles, California, 90033, USA.
Yuanpu ChiuCenter for Neurodegeneration and Regeneration, Zilkha Neurogenetic Institute, Department of Physiology and Biophysics, Keck School of Medicine, University of Southern California, Los Angeles, California, 90033, USA.
Ying QinCenter for Neurodegeneration and Regeneration, Zilkha Neurogenetic Institute, Department of Physiology and Biophysics, Keck School of Medicine, University of Southern California, Los Angeles, California, 90033, USA.
Zhen ZhaoCenter for Neurodegeneration and Regeneration, Zilkha Neurogenetic Institute, Department of Physiology and Biophysics, Keck School of Medicine, University of Southern California, Los Angeles, California, 90033, USA.

Funding

The role of ATP13A5 ATPase in determining blood-brain pericyte functionsRF1NS135617 · NINDS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ZHAO, ZHEN · 2023 to 2023
$2.4M
A TIMEM252-dependent Microvascular Endophenotype in Alzheimer’s DiseaseRF1NS122060 · NINDS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ZHAO, ZHEN · 2021 to 2021
$2.3M
Zika Virus Capsid Protein Mediated Blockage of host microRNA machineryR01NS110687 · NINDS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ZHAO, ZHEN · 2019 to 2023
$2.2M
Pericyte-neuronal crosstalk in health and Alzheimer's DiseaseR01AG061288 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ZHAO, ZHEN · 2019 to 2023
$2.1M
A TIMEM252-dependent Microvascular Endophenotype in Alzheimer’s DiseaseR01NS122060 · NINDS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ZHAO, ZHEN · 2024 to 2025
$1.5M
cGAS-STING mediated neuroinflammation in Alzheimer's diseaseR56AG082361 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI YUAN, WEIMING, ZHAO, ZHEN · 2023 to 2023
$826k
Probing the heterogeneity of brain pericytes using new genetic toolsR21AG085559 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ZHAO, ZHEN · 2024 to 2025
$456k
The molecular mechanism of PICALM-dependent endosomal traffickingR21AG066090 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ZHAO, ZHEN · 2019 to 2020
$454k
NIA NIH HHS R01 AG061288NIA NIH HHS R21 AG066090NIA NIH HHS R21 AG085559NIA NIH HHS R56 AG082361NINDS NIH HHS R01 NS110687NINDS NIH HHS R01 NS122060NINDS NIH HHS RF1 NS122060NINDS NIH HHS RF1 NS135617
6 · The paper itself

Abstract

Excessive inflammatory responses following traumatic brain injury (TBI) hinder tissue healing and impair long-term functional recovery. In addition to therapeutic strategies that directly target the core pathological mechanisms of TBI, biomaterials and regenerative medicine now offer promising new avenues. Here, we report a new formulation of an injectable hydrogel based on gelatin methacryloyl (GelMA) conjugated with β-cyclodextrin (βCD), designed for implantation in TBI lesions. Compared to GelMA alone, βCD-containing hydrogels (βCD-GelMA) demonstrated a strong capacity to sequester cholesterol from cultured cells, thereby reducing lipid droplet formation and suppressing inflammatory responses. Notably, aberrant cholesterol accumulation and lipid droplet formation were observed in a mouse model of TBI, andimplantation of βCD-GelMA into the lesion area significantly reduced peak tissue cholesterol and lipid droplet levels post-injury. More importantly, βCD-GelMA mitigated gliosis, reduced inflammation and scar formation, and improved functional outcomes in the TBI model. Mechanistically, by scavenging cholesterol from injured tissue, βCD-GelMA normalized microglial lipid droplet and promoted polarization toward a less inflammatory phenotype. In summary, our study highlights the strong therapeutic potential of βCD in restoring cholesterol homeostasis and resolving lipid droplet-associated inflammation, and demonstrates that the βCD-GelMA functional hydrogel represents a promising intervention strategy for head injuries.

Indexed as

cholesterolhydrogellipid dropletmicroglianeuroinflammationTraumatic brain injury (TBI)

Identifiers

PMID40857429
PMCPMC12363451

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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.