Evidence map›Paper›PMID 37450265›Full record

ArticleIn vitro cellular & developmental biology. Animal2023

DHA attenuates cartilage degeneration by mediating apoptosis and autophagy in human chondrocytes and rat models of osteoarthritis.

Haomiao Yu, Zishun Gong, Guodong Wang, Ruiqi Cao, Heyong Yin, Lifeng Ma, Ai Guo

Abstract read
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In one paragraph

Article in In vitro cellular & developmental biology. Animal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.7field-weighted citation impact, top 15% of its field
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

5 citing papers in PubMed, 7 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Haomiao YuDepartment of Orthopaedics, Beijing Friendship Hospital, Capital Medical University, Yongan Road 95, Xicheng Distinct, Beijing, 100050, People's Republic of China.
Zishun GongDepartment of Orthopaedics, Beijing Friendship Hospital, Capital Medical University, Yongan Road 95, Xicheng Distinct, Beijing, 100050, People's Republic of China.
Guodong WangDepartment of Orthopaedics, Beijing Tongren Hospital, Capital Medical University, Beijing, China.
Ruiqi CaoDepartment of Orthopaedics, Beijing Friendship Hospital, Capital Medical University, Yongan Road 95, Xicheng Distinct, Beijing, 100050, People's Republic of China.
Heyong YinDepartment of Orthopaedics, Beijing Friendship Hospital, Capital Medical University, Yongan Road 95, Xicheng Distinct, Beijing, 100050, People's Republic of China.
Lifeng MaDepartment of Orthopaedics, Beijing Friendship Hospital, Capital Medical University, Yongan Road 95, Xicheng Distinct, Beijing, 100050, People's Republic of China. osteoma@163.com.
Ai GuoDepartment of Orthopaedics, Beijing Friendship Hospital, Capital Medical University, Yongan Road 95, Xicheng Distinct, Beijing, 100050, People's Republic of China. guoaij@139.com.ORCID http://orcid.org/0000-0002-4042-5682
Capital Medical University · CNBeijing Tongren Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteoarthritis (OA) is a degenerative joint disease that usually occurs in the elderly, and docosahexaenoic acid (DHA) plays a therapeutic role in cardiovascular disease, diabetes, and rheumatoid arthritis (RA) with its anti-inflammatory and antioxidant effects. The objective of this study is to investigate the effect and mechanism of DHA on hypertrophic differentiation and senescence of OA chondrocytes to provide a theoretical basis for the effect of OA clinical treatment. A human OA chondrocyte model was established by IL-1β, and a rat model of OA was established by anterior cruciate ligament (ACL) transection and medial meniscectomy. The result showed DHA promoted chondrocyte proliferation and reduced apoptosis. Transmission electron microscopy (TEM) analysis showed that there were more autophagosomes in the cytoplasm under the treatment of DHA. Compared to the OA group, samples from the OA + DHA group showed thickened cartilage, reduced degeneration, and an increased rate of collagen II-positive cells, while the Mankin score was significantly lower. In addition, DHA decreased the expression of phosphorylated mammalian target of rapamycin (p-mTOR) and the ratio of light chain 3-I/II (LC3-I/II) and increased the expression of Beclin-1 and Bcl-2 measured by western blot analysis. Therefore, DHA promotes chondrocyte proliferation, reduces apoptosis, and increases autophagy in OA chondrocytes, a process that is accomplished by inhibiting the expression of mTOR, c-Jun N-terminal kinase (JNK), and p38 signaling pathways, providing new perspectives and bootstrap points for the prevention and treatment of OA.

Indexed as

Cartilage, ArticularOsteoarthritisAnimalsApoptosisAutophagyCartilageChondrocytesDocosahexaenoic AcidsHumansMammalsRatsTOR Serine-Threonine KinasesDocosahexaenoic AcidsTOR Serine-Threonine KinasesApoptosisAutophagyChondrocyteDocosahexaenoic acidOsteoarthritis

Identifiers

PMID37450265
OpenAlexW4384298221

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.