Evidence map›Paper›PMID 41046448›Full record

ArticleCartilage2025

FKBP38 Alleviates Osteoarthritis Progression by Inhibiting Chondrocyte Senescence.

Junfeng Wu, Wenping Chen, Zilin Zou, Honghao Li, Tao Zhou, Zhengquan Liao, Zhi Rao, Kai Li, Xinyu Tan, He Cao and 1 more

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Article in Cartilage, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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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3 · Its place in the literature

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0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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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.

Junfeng WuGuangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Academy of Orthopedics, Guangdong Province, Orthopedic Hospital of Guangdong Province, The Third School of Clinical Medicine, Southern Medical University, The Third Affiliated Hospital, Southern Medical University, Guangzhou, China.ORCID 0009-0007-9550-8278
Wenping ChenGuangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Academy of Orthopedics, Guangdong Province, Orthopedic Hospital of Guangdong Province, The Third School of Clinical Medicine, Southern Medical University, The Third Affiliated Hospital, Southern Medical University, Guangzhou, China.
Zilin ZouGuangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Academy of Orthopedics, Guangdong Province, Orthopedic Hospital of Guangdong Province, The Third School of Clinical Medicine, Southern Medical University, The Third Affiliated Hospital, Southern Medical University, Guangzhou, China.
Honghao LiGuangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Academy of Orthopedics, Guangdong Province, Orthopedic Hospital of Guangdong Province, The Third School of Clinical Medicine, Southern Medical University, The Third Affiliated Hospital, Southern Medical University, Guangzhou, China.
Tao ZhouGuangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Academy of Orthopedics, Guangdong Province, Orthopedic Hospital of Guangdong Province, The Third School of Clinical Medicine, Southern Medical University, The Third Affiliated Hospital, Southern Medical University, Guangzhou, China.
Zhengquan LiaoGuangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Academy of Orthopedics, Guangdong Province, Orthopedic Hospital of Guangdong Province, The Third School of Clinical Medicine, Southern Medical University, The Third Affiliated Hospital, Southern Medical University, Guangzhou, China.
Zhi RaoGuangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Academy of Orthopedics, Guangdong Province, Orthopedic Hospital of Guangdong Province, The Third School of Clinical Medicine, Southern Medical University, The Third Affiliated Hospital, Southern Medical University, Guangzhou, China.
Kai LiGuangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Academy of Orthopedics, Guangdong Province, Orthopedic Hospital of Guangdong Province, The Third School of Clinical Medicine, Southern Medical University, The Third Affiliated Hospital, Southern Medical University, Guangzhou, China.
Xinyu TanGuangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Academy of Orthopedics, Guangdong Province, Orthopedic Hospital of Guangdong Province, The Third School of Clinical Medicine, Southern Medical University, The Third Affiliated Hospital, Southern Medical University, Guangzhou, China.
He CaoGuangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Academy of Orthopedics, Guangdong Province, Orthopedic Hospital of Guangdong Province, The Third School of Clinical Medicine, Southern Medical University, The Third Affiliated Hospital, Southern Medical University, Guangzhou, China.ORCID 0000-0001-9151-0177
Hong WangGuangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Academy of Orthopedics, Guangdong Province, Orthopedic Hospital of Guangdong Province, The Third School of Clinical Medicine, Southern Medical University, The Third Affiliated Hospital, Southern Medical University, Guangzhou, China.ORCID 0009-0004-0295-7401

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ObjectiveOsteoarthritis (OA) is a prevalent age-related degenerative joint disease characterized by cartilage degeneration, joint pain, and reduced mobility, with aging as the primary risk factor. This study aimed to investigate the role and mechanism of FK506 binding protein 38 (FKBP38) in chondrocyte senescence and OA progression.MethodsFKBP38 expression was detected in articular cartilage from natural aging and OA mouse models. Mice with FKBP38 conditional knockout (FKBP38-cKO) and inducible conditional knockout (FKBP38-iKO) were generated for these models. An adeno-associated virus (AAV) vector overexpressing FKBP38 was injected into wild-type mouse joints. Joint damage was assessed at 8 and 18 months for natural aging or 4 and 8 weeks after DMM surgery by histology.ResultsFKBP38 expression was downregulated in cartilage from both natural aging and OA mice. FKBP38 overexpression protected against H2O2-induced senescence in chondrocytes. Addition of rapamycin to inhibit mTORC1 signaling rescued the enhanced senescence and catabolism caused by FKBP38 knockdown in chondrocytes. Conditional deletion of FKBP38 in chondrocytes significantly accelerated senescence and aggravated both natural aging and OA progression by activating mTORC1 signaling, whereas overexpression of FKBP38 delayed these processes.ConclusionThese results indicate that FKBP38 protects against chondrocyte senescence and cartilage degradation to alleviate OA progression by inhibiting mTORC1 signaling.

Indexed as

cartilagechondrocytes senescenceFK506-binding protein 38mTORC1 signalingosteoarthritis

Identifiers

PMID41046448
PMCPMC12497730

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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.