Evidence map›Paper›PMID 42290977›Full record

ArticleBioactive materials2026

A cell-free lipid sterosomal therapeutic enables bone regeneration via USP18-mediated noncanonical S1P signaling.

Wen-Hao Ye, Jie Zhou, Junxiang Qiu, Zhengbo Liu, Ruolin He, Sixu Chen, Jing Wen, Binyang Feng, Beibei Lyu, Zhen Wang and 1 more

Abstract read
In one paragraph

Article in Bioactive materials, 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

11 authors.

Wen-Hao YeGuangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Cell Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.
Jie ZhouGuangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Cell Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.
Junxiang QiuGuangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Cell Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.
Zhengbo LiuGuangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Cell Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.
Ruolin HeGuangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Cell Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.
Sixu ChenAcademy of Orthopedics Guangdong Province, Orthopedic Hospital of Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Guangzhou, 510630, China.
Jing WenGuangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Cell Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.
Binyang FengGuangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Cell Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.
Beibei LyuGuangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Cell Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.
Zhen WangGuangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Cell Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.
Zhong-Kai CuiGuangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Cell Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Effective treatment of critical-sized bone defects remains challenging due to impaired osteogenesis, insufficient vascularization and oxidative stress-induced cell loss. Here, we report a chemically defined, cell-free sterosomal nanoplatform composed of sphingosine-1-phosphate (S1P) and 20(S)-hydroxycholesterol (Oxy) that integrates cytoprotective, pro-angiogenic, and osteogenic functions. S1P/Oxy sterosomes simultaneously enhance osteogenic differentiation and endothelial angiogenic activity while protecting resident cells from oxidative stress. In a rat critical-sized calvarial defect model, local administration of sterosomes promoted robust and spatially organized bone regeneration, without exogenous cells or growth factors. Mechanistically, transcriptomic and functional analyses identified ubiquitin-specific peptidase 18 (USP18) as a novel and essential mediator of sterosomal S1P-induced osteogenesis, independent of canonical S1P receptors. Notably, this effect is observed only when S1P is presented in a sterosomal assembly rather than in its free molecular form. Our work establishes a cell-free sterosomal strategy for effective bone regeneration accompanied by functional neovascularization and discovered a novel intracellular actuator for S1P.

Indexed as

Microenvironment-adaptiveSelf-therapeuticSphingosine-1-phosphateSterosomesVascularized bone regeneration

Identifiers

PMID42290977
PMCPMC13264244

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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 OpenQuestion graph.