Evidence map›Paper›PMID 38265688›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2024

Mammalian STE20-like kinase 1 inhibits synoviocytes activation in rheumatoid arthritis through mitochondrial dysfunction mediated by SIRT3/mTOR axis.

Min Tan, Jing Mao, Jianxiong Zheng, Yu Meng, Jun Li, Jiayao Hao, Haili Shen

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Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2024. 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
1.4field-weighted citation impact, top 21% 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, 6 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.

Min TanDepartment of Rheumatology, Lanzhou University Second Hospital, No. 82, Cui Ying Men Street, Lanzhou City, 730030, Gansu Province, People's Republic of China.
Jing MaoDepartment of Rheumatology, Lanzhou University Second Hospital, No. 82, Cui Ying Men Street, Lanzhou City, 730030, Gansu Province, People's Republic of China.
Jianxiong ZhengDepartment of Rheumatology, Lanzhou University Second Hospital, No. 82, Cui Ying Men Street, Lanzhou City, 730030, Gansu Province, People's Republic of China.
Yu MengDepartment of Pain, Lanzhou University Second Hospital, Lanzhou, People's Republic of China.
Jun LiDepartment of Rheumatology, Lanzhou University Second Hospital, No. 82, Cui Ying Men Street, Lanzhou City, 730030, Gansu Province, People's Republic of China.
Jiayao HaoDepartment of Rheumatology, Lanzhou University Second Hospital, No. 82, Cui Ying Men Street, Lanzhou City, 730030, Gansu Province, People's Republic of China.
Haili ShenDepartment of Rheumatology, Lanzhou University Second Hospital, No. 82, Cui Ying Men Street, Lanzhou City, 730030, Gansu Province, People's Republic of China. shenhl@lzu.edu.cn.
Lanzhou University · CNLanzhou University Second Hospital · CN

Funding

National Natural Science Foundation of China 81960302Natural Science Foundation of Gansu Province 22JR5RA975Science and Technology Program of Gansu Province 21JR7RA437
6 · The paper itself

Abstract

backgroundMammalian STE20-like kinase 1 (MST1) is involved in the occurrence of cancer and autoimmune diseases by regulating cell proliferation, differentiation, apoptosis and other functions. However, its role and downstream targets in rheumatoid arthritis (RA) remain unclear.

methodsThe model of RA fibroblast-like synoviocytes (RA-FLSs) overexpressing MST1 was constructed by lentiviral transfection in vitro and analyzed the effects of MST1 on apoptosis, migration, invasion, and inflammation of RA-FLSs. The effect of MST1 on joint synovial membrane inflammation and bone destruction was observed in vivo by establishing a rat model of arthritis with complete Freund's adjuvant.

resultsMST1 is down-regulated in RA-FLSs, and up-regulation of MST1 inhibits the survival, migration, invasion and inflammation of RA-FLSs. Mechanistically, MST1 inhibits SIRT3/mTOR-signaling pathway, inducing decreased mitochondrial autophagy and increased mitochondrial fission, resulting in mitochondrial morphological abnormalities and dysfunction, and ultimately increased apoptosis. We have observed that activation of MST1 alleviates synovial inflammation and bone erosion in vivo.

conclusionsMST1 reduces the survival, migration, invasion and inflammation of FLSs by inhibiting the SIRT3/mTOR axis to reduce mitochondrial autophagy and promote mitochondrial division, thereby achieving the potential role of relieving rheumatoid arthritis.

Indexed as

Arthritis, RheumatoidMitochondrial DiseasesSirtuin 3SynoviocytesAnimalsCell ProliferationCells, CulturedFibroblastsHippo KinasesInflammationMammalsRatsTOR Serine-Threonine KinasesHippo KinasesmTOR protein, ratSirtuin 3Stk4 protein, ratTOR Serine-Threonine KinasesFibroblast-like synoviocytesMammalian STE20-like kinase 1Mitochondrial dysfunctionRheumatoid arthritisSIRT3/mTOR axis

Identifiers

PMID38265688
OpenAlexW4391169047

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.