Evidence map›Paper›PMID 36625319›Full record

ArticleMolecules and cells2023

RUNX1 Ameliorates Rheumatoid Arthritis Progression through Epigenetic Inhibition of LRRC15.

Hao Ding, Xiaoliang Mei, Lintao Li, Peng Fang, Ting Guo, Jianning Zhao

Open access · diamondAbstract read
In one paragraph

Article in Molecules and cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
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  10. Molecules (Basel, Switzerland) · 2024
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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

6 authors at 2 institutions in 1 country.

Hao DingDepartment of Orthopedics, Jinling Hospital, Jinling Clinical Medical College of Nanjing Medical University, Nanjing 211166, China.ORCID https://orcid.org/0000-0003-2688-3852
Xiaoliang MeiDepartment of Orthopedics, The Affiliated Taizhou People's Hospital of Nanjing Medical University, Taizhou 225300, China.ORCID https://orcid.org/0000-0002-3576-0419
Lintao LiDepartment of Orthopedics, Jinling Hospital, Jinling Clinical Medical College of Nanjing Medical University, Nanjing 211166, China.ORCID https://orcid.org/0000-0002-1298-2561
Peng FangDepartment of Orthopedics, Jinling Hospital, Jinling Clinical Medical College of Nanjing Medical University, Nanjing 211166, China.ORCID https://orcid.org/0000-0002-8684-2756
Ting GuoDepartment of Orthopedics, Jinling Hospital, Jinling Clinical Medical College of Nanjing Medical University, Nanjing 211166, China.ORCID https://orcid.org/0000-0002-7815-9033
Jianning ZhaoDepartment of Orthopedics, Jinling Hospital, Jinling Clinical Medical College of Nanjing Medical University, Nanjing 211166, China.ORCID https://orcid.org/0000-0003-3950-9974
Nanjing General Hospital of Nanjing Military Command · CNNantong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Leucine-rich repeat containing 15 (LRRC15) has been identified as a contributing factor for cartilage damage in osteoarthritis; however, its involvement in rheumatoid arthritis (RA) and the underlying mechanisms have not been well characterized. The purpose of this study was to explore the function of LRRC15 in RA-associated fibroblast-like synoviocytes (RA-FLS) and in mice with collagen-induced arthritis (CIA) and to dissect the epigenetic mechanisms involved. LRRC15 was overexpressed in the synovial tissues of patients with RA, and LRRC15 overexpression was associated with increased proliferative, migratory, invasive, and angiogenic capacities of RA-FLS and accelerated release of pro-inflammatory cytokines. LRRC15 knockdown significantly inhibited synovial proliferation and reduced bone invasion and destruction in CIA mice. Runt-related transcription factor 1 (RUNX1) transcriptionally represses LRRC15 by binding to core-binding factor subunit beta (CBF-β). Overexpression of RUNX1 significantly inhibited the invasive phenotype of RA-FLS and suppressed the expression of proinflammatory cytokines. Conversely, the effects of RUNX1 were significantly reversed after overexpression of LRRC15 or inhibition of RUNX1-CBF-β interactions. Therefore, we demonstrated that RUNX1-mediated transcriptional repression of LRRC15 inhibited the development of RA, which may have therapeutic effects for RA patients.

Indexed as

Arthritis, ExperimentalArthritis, RheumatoidAnimalsCell MovementCell ProliferationCells, CulturedCore Binding Factor Alpha 2 SubunitCytokinesEpigenesis, GeneticFibroblastsHumansMembrane ProteinsMiceSynovial MembraneCore Binding Factor Alpha 2 SubunitCytokinesLRRC15 protein, humanLrrc15 protein, mouseMembrane ProteinsRUNX1 protein, humanRunx1 protein, mouseepigeneticfibroblast-like synoviocytesLRRC15rheumatoid arthritisRUNX1

Identifiers

PMID36625319
PMCPMC10086557
OpenAlexW4315436678

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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 OpenQuestion graph.