Evidence map›Paper›PMID 40055825›Full record

ArticleArthritis research & therapy2025

SDF-1 alleviates osteoarthritis by resolving mitochondrial dysfunction through the activation of the Sirt3/PGC-1α signalling pathway.

Yanping Zhao, Dan Lin, Xiaoying Zhu, Jingyao Yan, Yan Liang, Yanli Wang, Tianqi Dai, Zhiyi Zhang, Shuya Wang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Arthritis research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Roles of SIRT3 in aging and aging-related diseases.International journal of biological sciences · 2025
    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

9 authors.

Yanping ZhaoDepartment of Rheumatology, The Affiliated hospital of Harbin Medical University, NO.23 Youzheng St, Harbin, 150001, China.
Dan LinDepartment of Rheumatology, The Affiliated hospital of Harbin Medical University, NO.23 Youzheng St, Harbin, 150001, China.
Xiaoying ZhuDepartment of Rheumatology, The Affiliated hospital of Harbin Medical University, NO.23 Youzheng St, Harbin, 150001, China.
Jingyao YanDepartment of Rheumatology, The Affiliated hospital of Harbin Medical University, NO.23 Youzheng St, Harbin, 150001, China.
Yan LiangDepartment of Rheumatology, The Affiliated hospital of Harbin Medical University, NO.23 Youzheng St, Harbin, 150001, China.
Yanli WangDepartment of Rheumatology, The Affiliated hospital of Harbin Medical University, NO.23 Youzheng St, Harbin, 150001, China.
Tianqi DaiDepartment of Rheumatology, The Affiliated hospital of Harbin Medical University, NO.23 Youzheng St, Harbin, 150001, China.
Zhiyi ZhangDepartment of Rheumatology, The Affiliated hospital of Harbin Medical University, NO.23 Youzheng St, Harbin, 150001, China. zhangzhiyi2014@163.com.
Shuya WangDepartment of Rheumatology, The Affiliated hospital of Harbin Medical University, NO.23 Youzheng St, Harbin, 150001, China. 13804539667@163.com.

Funding

the First Affiliated Hospital of HMU Merit Review Frontiers grant HYD2020YQ0008the National Natural Science Foundation of China NSFC 82202020
6 · The paper itself

Abstract

objectiveOsteoarthritis (OA) is the most common form of joint disease. Currently, OA treatment is limited to controlling symptoms. Our previous study showed that stromal cell-derived factor 1 (SDF-1) delayed the progression of OA to a certain extent. The aim of this study was to explore the specific mechanism of SDF-1 in OA. MATERIALS AND

methodsOA chondrocytes and a collagen-induced osteoarthritis (CIOA) mouse model were used as in vitro and in vivo models, respectively. SDF-1 was used to treat OA in vitro and in vivo. To explore the mechanism of SDF-1 in OA treatment, we pretreated chondrocytes with a Sirt 3 inhibitor and assessed mitochondrial function and then analysed related indicators of cartilage anabolic and cartilage metabolism.

resultsSOD2 and PGC-1α levels were significantly lower in OA chondrocytes and the cartilage of CIOA model mice than in normal chondrocytes, and mitochondrial dysfunction occurred in OA. After treating OA chondrocytes and CIOA model mice with exogenous SDF-1, mitochondrial dysfunction and abnormal biomarkers of OA normalized. The pretreatment of OA chondrocytes with a Sirt 3 inhibitor or mitochondrial function inhibitor before SDF-1 exposure reversed these changes.

conclusionsSDF-1 can alleviate OA by resolving mitochondrial dysfunction through the activation of the Sirt3/PGC-1α signalling pathway, and therefore, SDF-1 may be a good candidate as a new treatment for OA.

Indexed as

Chemokine CXCL12MitochondriaOsteoarthritisPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaSirtuin 3AnimalsCells, CulturedChondrocytesHumansMaleMiceMice, Inbred C57BLSignal TransductionChemokine CXCL12Cxcl12 protein, mousePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, mouseSirt3 protein, mouseSirtuin 3ChondrocyteMitochondrial dysfunctionOsteoarthritisSirt3Stromal cell-derived factor 1

Identifiers

PMID40055825
PMCPMC11887228

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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.