Evidence map›Paper›PMID 41535892›Full record

ArticleArthritis research & therapy2026

FSCN1 induces subchondral bone sclerosis in osteoarthritis via modulating actin cytoskeleton dynamics and YAP signaling.

Yun Xiao, Liangyu Chen, Dalin Chen, Jiamin Li, Qinwei Cheng, Panpan Yang, Zilin Zou, Junfeng Wu, Kai Li, Chengliang Yang and 2 more

Abstract read
In one paragraph

Article in Arthritis research & therapy, 2026. 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

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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

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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. Review
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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

12 authors.

Yun Xiao *Academy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, The Third School of Clinical Medicine, Southern Medical University, The Third Affiliated Hospital, Southern Medical University, Guangdong, 510630, Guangzhou, China.
Liangyu Chen *Academy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, The Third School of Clinical Medicine, Southern Medical University, The Third Affiliated Hospital, Southern Medical University, Guangdong, 510630, Guangzhou, China.
Dalin Chen *Academy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, The Third School of Clinical Medicine, Southern Medical University, The Third Affiliated Hospital, Southern Medical University, Guangdong, 510630, Guangzhou, China.
Jiamin LiDepartment of Orthopedics, Affiliated Hospital of Youjiang Medical University for Nationalities, Guangxi Key Laboratory for Biomedical Materials Research, Guangxi, 533000, Baise, China.
Qinwei ChengAcademy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, The Third School of Clinical Medicine, Southern Medical University, The Third Affiliated Hospital, Southern Medical University, Guangdong, 510630, Guangzhou, China.
Panpan YangAcademy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, The Third School of Clinical Medicine, Southern Medical University, The Third Affiliated Hospital, Southern Medical University, Guangdong, 510630, Guangzhou, China.
Zilin ZouAcademy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, The Third School of Clinical Medicine, Southern Medical University, The Third Affiliated Hospital, Southern Medical University, Guangdong, 510630, Guangzhou, China.
Junfeng WuAcademy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, The Third School of Clinical Medicine, Southern Medical University, The Third Affiliated Hospital, Southern Medical University, Guangdong, 510630, Guangzhou, China.
Kai LiAcademy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, The Third School of Clinical Medicine, Southern Medical University, The Third Affiliated Hospital, Southern Medical University, Guangdong, 510630, Guangzhou, China.
Chengliang YangDepartment of Orthopedics, Affiliated Hospital of Youjiang Medical University for Nationalities, Guangxi Key Laboratory for Biomedical Materials Research, Guangxi, 533000, Baise, China. yangchengliang@ymcn.edu.cn.
Hong WangAcademy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, The Third School of Clinical Medicine, Southern Medical University, The Third Affiliated Hospital, Southern Medical University, Guangdong, 510630, Guangzhou, China. wh540102@163.com.
Changsheng YangAcademy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, The Third School of Clinical Medicine, Southern Medical University, The Third Affiliated Hospital, Southern Medical University, Guangdong, 510630, Guangzhou, China. yeahchangsheng@163.com.

Funding

Basic and Applied Basic Research Foundation of Guangdong Province 2025A1515012627Medical Scientific Research Foundation of Guangdong Province A2024368Natural Science Foundation of Guangxi Province 2025GXNSFHA069017
6 · The paper itself

Abstract

backgroundSubchondral bone is a dynamic tissue maintained by bone remodeling and responded rapidly to mechanical loading, which is strongly associated with cartilage degradation in osteoarthritis (OA), but the underlying mechanisms of which is still blurring.

methodsExperimental OA mice models were generated by mechanical overload with 60 cycles of 14 N axial compressive loads twice a week or anterior cruciate ligament transection surgery. FSCN1 expression was evaluated in subchondral bone from experimental OA mice and human OA. Mice with FSCN1 conditional knockout in pre-osteoblasts were generated, and adeno-associated virus expressing FSCN1 was injected intra-articularly in mice. Therapeutic efficacy of FSCN1 inhibitor NP-G2-044 was determined in OA mice.

resultsIncreased FSCN1 expression was positively associated with osteogenesis and subchondral bone sclerosis induced by mechanical loading. Deletion of FSCN1 in pre-osteoblasts delays osteogenesis and prevents abnormal subchondral bone sclerosis, whereas overexpression of FSCN1 exacerbates this. Under the stimulation of mechanical stress, Ras homologue gene family member A in osteoblasts competitively binds with protein kinase C to FSCN1, thereby inhibiting FSCN1 phosphorylation and promoting cytoskeleton formation, thereby activating Hippo/YAP signaling to increase metabolic activity of osteoblasts. These abnormal osteoblasts secrete more osteogenesis proteins, including osteopontin, leading to subchondral bone sclerosis and cartilage erosion, thus aggravating the progression of OA. Furthermore, we confirmed that the inhibitor of FSCN1, NP-G2-044 effectively attenuates subchondral bone sclerosis and OA progression in mice.

conclusionsThis study suggests that FSCN1 is a key factor in the relationship between mechanical stress, actin cytoskeleton dynamic, subchondral bone sclerosis and OA pathology. Targeting FSCN1 represents a promising pharmacological approach for OA therapy.

Indexed as

Actin CytoskeletonAdaptor Proteins, Signal TransducingCarrier ProteinsMicrofilament ProteinsOsteoarthritisAnimalsBone and BonesCell Cycle ProteinsDisease Models, AnimalHumansMaleMiceMice, Inbred C57BLMice, KnockoutOsteoblastsOsteogenesisAdaptor Proteins, Signal TransducingCarrier ProteinsCell Cycle ProteinsMicrofilament ProteinsYap1 protein, mouseYAP-Signaling ProteinsFSCN1Hippo/YAP signalingMechanical stressOsteoarthritisSubchondral bone

Identifiers

PMID41535892
PMCPMC12892604

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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.