Evidence map›Paper›PMID 39262222›Full record

ArticleArthritis & rheumatology (Hoboken, N.J.)2025

Enhancement of Intracellular Cholesterol Efflux in Chondrocytes Leading to Alleviation of Osteoarthritis Progression.

Gyuseok Lee, Jiye Yang, Su-Jin Kim, Thanh-Tam Tran, Sun Young Lee, Ka Hyon Park, Seung-Hee Kwon, Ki-Ho Chung, Jeong-Tae Koh, Yun Hyun Huh and 4 more

Abstract read
In one paragraph

Article in Arthritis & rheumatology (Hoboken, N.J.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

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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

14 authors.

Gyuseok LeeChonnam National University, Gwangju, Republic of Korea.
Jiye YangGwangju Institute of Science and Technology, Gwangju, Republic of Korea.
Su-Jin KimChonnam National University, Gwangju, Republic of Korea.
Thanh-Tam TranChonnam National University, Gwangju, Republic of Korea.
Sun Young LeeChonnam National University, Gwangju, Republic of Korea.
Ka Hyon ParkChonnam National University, Gwangju, Republic of Korea.
Seung-Hee KwonChonnam National University, Gwangju, Republic of Korea.
Ki-Ho ChungChonnam National University, Gwangju, Republic of Korea.
Jeong-Tae KohChonnam National University, Gwangju, Republic of Korea.
Yun Hyun HuhGwangju Institute of Science and Technology, Gwangju, Republic of Korea.
Jong-Keun SeonChonnam National University Hwasun Hospital and Medical School, Hwasun, Republic of Korea.ORCID 0000-0002-6920-5659
Hyun Ah KimHallym University, Sacred Heart Hospital, Anyang, Republic of Korea.
Jang-Soo ChunGwangju Institute of Science and Technology, Gwangju, Republic of Korea.ORCID 0000-0003-2910-181X
Je-Hwang RyuChonnam National University, Gwangju, Republic of Korea.ORCID 0000-0002-8708-8943

Funding

Korean Fund for Regenerative MedicineKorean governmentMinistry of Science and ICT, the Ministry of Health and Welfare 22A0104L1National Research Foundation of Korea 2019R1A5A2027521National Research Foundation of Korea 2021R1A2C3005727National Research Foundation of Korea 2021R1I1A1A01061246
6 · The paper itself

Abstract

objectiveOsteoarthritis (OA) is the most common degenerative disease worldwide, with no practical means of prevention and limited treatment options. Recently, our group unveiled a novel mechanism contributing to OA pathogenesis in association with abnormal cholesterol metabolism in chondrocytes. In this study, we aimed to establish a clinical link between lipid profiles and OA in humans, assess the effectiveness of cholesterol-lowering drugs in suppressing OA development in mice, and uncover the cholesterol-lowering mechanisms that effectively impede OA progression.

methodsFive clinically approved cholesterol-lowering drugs (fenofibrate, atorvastatin, ezetimibe, niacin, and lomitapide) were injected into the knee joints or administered with diet to mice with OA who underwent destabilization of the medial meniscus induction and were fed a 2% high-cholesterol diet. Gene expression linked to cholesterol metabolism was determined using microarray analysis. Furthermore, the in vivo functions of these genes were explored through intra-articular injection of either its inhibitor or adenovirus.

resultsLogistic regression analysis confirmed a close relationship between the diagnostic criteria of hyperlipidemia based on serum lipid levels and OA incidence. Among the cholesterol-lowering drugs examined, fenofibrate exerted the most significant protective effect against cartilage destruction, which was attributed to elevated levels of high-density lipoprotein cholesterol that are crucial for cholesterol efflux. Notably, cholesterol efflux was suppressed during OA progression via down-regulation of apolipoprotein A1-binding protein (AIBP) expression. Overexpression of AIBP effectively inhibits OA progression.

conclusionOur results suggest that restoration of cholesterol homeostasis to a normal state through administration of fenofibrate or AIBP overexpression, both of which induce cholesterol efflux, offers an effective therapeutic option for patients with OA.

Indexed as

Anticholesteremic AgentsCholesterolChondrocytesOsteoarthritisOsteoarthritis, KneeAnimalsAtorvastatinBenzimidazolesDisease ProgressionEzetimibeFenofibrateHumansMaleMiceMice, Inbred C57BLNiacinAnticholesteremic AgentsAtorvastatinBenzimidazolesCholesterolEzetimibeFenofibrateNiacin

Identifiers

PMID39262222
PMCPMC11782112

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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.