Evidence map›Paper›PMID 42666098›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

BAP31 Drives Cartilage Calcification through Disruption of Autophagosome-Lysosome Fusion in Osteoarthritis.

Zhi-Hua Xu, Ruo-Xin Wang, Feng He, Qian Liu, Fu-Yin Li, Min Hui, Yu-Qian Shi, Yu Jiang, Qing-Hua Li, Jun-Wen Jing and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 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

14 authors.

Zhi-Hua Xu *State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi International Joint Research Center For Oral Diseases, Department of Oral Anatomy and Physiology, School of Stomatology, The Fourth Military Medical University, Xi'an, China.
Ruo-Xin Wang *State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Clinical Research Center for Oral Diseases, Department of Orthodontics, School of Stomatology, The Fourth Military Medical University, Xi'an, China.
Feng He *State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Key Laboratory of Stomatology, Department of Oral and Maxillofacial Surgery, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, China.
Qian Liu *Department of Stomatology, Air Force Medical Center, Air Force Medical University, PLA, Beijing, China.
Fu-Yin Li *State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi International Joint Research Center For Oral Diseases, Department of Oral Anatomy and Physiology, School of Stomatology, The Fourth Military Medical University, Xi'an, China.
Min HuiSchool of Medicine, Northwest University, Xi'an, Shaanxi, China.
Yu-Qian ShiState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi International Joint Research Center For Oral Diseases, Department of Oral Anatomy and Physiology, School of Stomatology, The Fourth Military Medical University, Xi'an, China.
Yu JiangDepartment of Pharmacology, Shaanxi University of Chinese Medicine, Xianyang, Shaanxi, China.
Qing-Hua LiState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi International Joint Research Center For Oral Diseases, Department of Oral Anatomy and Physiology, School of Stomatology, The Fourth Military Medical University, Xi'an, China.
Jun-Wen JingState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi International Joint Research Center For Oral Diseases, Department of Oral Anatomy and Physiology, School of Stomatology, The Fourth Military Medical University, Xi'an, China.
Shi-Bin YuState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi International Joint Research Center For Oral Diseases, Department of Oral Anatomy and Physiology, School of Stomatology, The Fourth Military Medical University, Xi'an, China.
Li-Tian MaDepartment of Thoracic Surgery, Tangdu Hospital, Air Force Medical University, Xi'an, Shaanxi, China.ORCID https://orcid.org/0000-0002-7177-4439
Qian-Nan NiuState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Clinical Research Center for Oral Diseases, Department of Orthodontics, School of Stomatology, The Fourth Military Medical University, Xi'an, China.
Mian ZhangState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi International Joint Research Center For Oral Diseases, Department of Oral Anatomy and Physiology, School of Stomatology, The Fourth Military Medical University, Xi'an, China.ORCID https://orcid.org/0000-0003-2464-361X

Funding

Basic Research Program of Natural Science in Shaanxi Province 2025JC-YBQN-1159BioRender under Academic Publication License WO28S6017ZNational Natural Science Foundation of China 82301111National Natural Science Foundation of China 82301121National Natural Science Foundation of China 82401153
6 · The paper itself

Abstract

Pathological cartilage calcification represents a pivotal pathological alteration in osteoarthritis (OA), yet its underlying mechanisms remain poorly understood. Exosomes are involved in facilitating calcification, and their biogenesis may be linked to autophagy disruption. However, whether autophagy disruption regulates exosome-mediated calcification in OA remains to be elucidated. Here, B-cell receptor-associated protein 31 (BAP31) was identified as a key mechanosensitive regulator bridging this gap. Mechanical stimulation activated BAP31 in chondrocytes. Protein docking, coimmunoprecipitation assays, and competitive pull-down assays demonstrated that activated BAP31 competes with autophagy-related 14 (ATG14) for binding to syntaxin 17 (STX17), thereby disrupting the STX17-ATG14 complex, which is essential for autophagosome‒lysosome fusion. This disruption led to the accumulation of autophagosomes, which in turn drove the release of exosomes that facilitated pathological cartilage calcification. Critically, intra-articular delivery of adeno-associated virus-mediated BAP31 shRNA restored autophagosome‒lysosome fusion, suppressed exosome release, and attenuated cartilage calcification and degeneration in a rat OA model. Collectively, these findings identify BAP31 as a mechanical stress-responsive switch that couples impaired autophagy to exosome-mediated calcification, highlighting its potential as a therapeutic target for OA.

Indexed as

autophagy, BAP31exosomeosteoarthritispathological calcification

Identifiers

PMID42666098
PMCPMC13525426

What OpenQuestion holds

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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.