Evidence map›Paper›PMID 39126207›Full record

ArticleAging cell2024

β-Hydroxybutyrate enhances chondrocyte mitophagy and reduces cartilage degeneration in osteoarthritis via the HCAR2/AMPK/PINK1/Parkin pathway.

Huangming Zhuang, Xunshan Ren, Yuelong Zhang, Huajie Li, Panghu Zhou

Abstract read
In one paragraph

Article in Aging cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing 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

30 citing papers in PubMed.

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  4. [Protective effect and mechanism of TSPAN9-mediated mitocytosis in interleukin-1β-induced rat chondrocyte senescence].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2026
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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

5 authors.

Huangming ZhuangDepartment of Orthopedics, Renmin Hospital of Wuhan University, Wuhan, China.
Xunshan RenDepartment of Orthopedics, Renmin Hospital of Wuhan University, Wuhan, China.
Yuelong ZhangDepartment of Orthopedics, Renmin Hospital of Wuhan University, Wuhan, China.
Huajie LiDepartment of Orthopedics, Renmin Hospital of Wuhan University, Wuhan, China.
Panghu ZhouDepartment of Orthopedics, Renmin Hospital of Wuhan University, Wuhan, China.ORCID 0000-0002-7020-4258

Funding

Cross-Innovation Talent Program of Renmin Hospital of Wuhan University JCRCFZ-2022-019Fundamental Research Funds for the Central Universities 2042023kf0224Hubei Medical Youth Tip-Top Talent to Panghu zhou CZ2024020005-11National Natural Science Foundation of China 82372489Wuhan University Education and Development Foundation 2002330
6 · The paper itself

Abstract

Osteoarthritis (OA) is widely recognized as the prevailing joint disease associated with aging. The ketogenic diet (KD) has been postulated to impede the advancement of various inflammatory ailments. β-Hydroxybutyrate (βOHB), a prominent constituent of ketone bodies, has recently been proposed to possess crucial signaling capabilities. In this study, we propose to explore the role and mechanism of βOHB in OA. Tissue staining and inflammatory factor assay were employed to evaluate the impacts of KD and βOHB on OA rats. The oxidative stress conditions in chondrocytes were induced using tert-butyl hydroperoxide (TBHP). The mechanisms were determined using the siRNA of hydroxycarboxylic acid receptor 2 (HCAR2), the antagonist of adenosine monophosphate-activated protein kinase (AMPK), and the inhibitor of mitophagy. The administration of KD demonstrated a reduction in pathological damage to cartilage, as well as a decrease in plasma levels of inflammatory factors. Furthermore, it resulted in an increase in the concentration of βOHB in the blood and synovial fluid. In vitro experiments showed that βOHB facilitated mitophagy and adenosine triphosphate production. Besides, βOHB mitigated chondrocyte senescence, inflammatory factors secretion, extracellular matrix degradation, and apoptosis induced by TBHP. Subsequent investigations indicated that the protective effects of βOHB were no longer observed following the knockdown of HCAR2, the antagonist of AMPK, or the inhibitor of mitophagy. Moreover, in vivo studies suggested that βOHB played a protective role by targeting the HCAR2-AMPK-PINK1 axis. In conclusion, βOHB enhanced chondrocyte mitophagy through the HCAR2/AMPK/PINK1/Parkin pathway, offering a potential therapeutic approach for the treatment of OA.

Indexed as

3-Hydroxybutyric AcidAMP-Activated Protein KinasesChondrocytesMitophagyOsteoarthritisProtein KinasesUbiquitin-Protein LigasesAnimalsMalePTEN-Induced Putative KinaseRatsRats, Sprague-DawleyReceptors, G-Protein-CoupledSignal Transduction3-Hydroxybutyric AcidAMP-Activated Protein Kinasesparkin proteinProtein KinasesPTEN-Induced Putative KinaseReceptors, G-Protein-CoupledUbiquitin-Protein Ligaseshydroxycarboxylic acid receptor 2mitophagyosteoarthritissenescenceβ‐Hydroxybutyrate

Identifiers

PMID39126207
PMCPMC11561673

What Socratic holds

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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 Socratic graph.