Evidence map›Paper›PMID 41133454›Full record

ArticleInternational journal of molecular medicine2026

Targeting of CIRP attenuates osteoarthritis progression via suppressing TLR4/NF‑κB/NLRP3 signaling axis.

Weichao Sun, Yi Liao, Jianguo Feng, Jianhui Liang, Qifei He, Yinxing Cui, Dixi Huang, Houyin Shi, Wei You, Wei Sun and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Review
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

11 authors.

Weichao Sun *Department of Orthopedics, Shenzhen Second People's Hospital/First Affiliated Hospital of Shenzhen University Health Science Center, Shenzhen, Guangdong 518035, P.R. China.
Yi Liao *Department of Technical Support, The People's Hospital of Guangxi Zhuang Autonomous Region, Guangxi Academy of Medical Sciences, Nanning, Guangxi 530021, P.R. China.
Jianguo FengDepartment of Anesthesiology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646099, P.R. China.
Jianhui LiangDepartment of Orthopedics, Shenzhen Second People's Hospital/First Affiliated Hospital of Shenzhen University Health Science Center, Shenzhen, Guangdong 518035, P.R. China.
Qifei HeDepartment of Orthopedics, Shenzhen Second People's Hospital/First Affiliated Hospital of Shenzhen University Health Science Center, Shenzhen, Guangdong 518035, P.R. China.
Yinxing CuiDepartment of Physiology, School of Basic Medical Science, Southwest Medical University, Luzhou, Sichuan 646099, P.R. China.
Dixi HuangDepartment of Orthopedics, Shenzhen Second People's Hospital/First Affiliated Hospital of Shenzhen University Health Science Center, Shenzhen, Guangdong 518035, P.R. China.
Houyin ShiDepartment of Orthopedics, The Affiliated Traditional Chinese Medicine Hospital of Southwest Medical University, Luzhou, Sichuan 646000, P.R. China.
Wei YouDepartment of Orthopedics, Shenzhen Second People's Hospital/First Affiliated Hospital of Shenzhen University Health Science Center, Shenzhen, Guangdong 518035, P.R. China.
Wei SunDepartment of Orthopedics, Shenzhen Second People's Hospital/First Affiliated Hospital of Shenzhen University Health Science Center, Shenzhen, Guangdong 518035, P.R. China.
Qian YiDepartment of Physiology, School of Basic Medical Science, Southwest Medical University, Luzhou, Sichuan 646099, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteoarthritis (OA) is one of the most common joint diseases worldwide. Recently, cold‑inducible RNA binding protein (CIRP), a novel identified pro‑inflammatory cytokine, was reportedly increased in the synovial fluid of OA patients. However, its function and the underlying mechanism in OA progression remains unclear. Therefore, the current study investigated the role of CIRP in the progression of OA. It was observed that CIRP and matrix metalloproteinases were highly expressed in OA chondrocytes, whereas collagen Ⅱ exhibited low expression levels. Additionally, CIRP was found to be secreted by OA human chondrocytes in the form of exosomes. CIRP treatment influenced inflammatory related signaling pathway, which in turn affected inflammatory response and extracellular matrix (ECM) degradation in human chondrocytes. Additionally, CIRP induced the nuclear translocation of p65 and promoted ECM degradation dependent the Toll‑like receptor 4 (TLR4)/NF‑κB signaling. The present study also reported that CIRP increased the IL‑1β secretion via the NLR family pyrin domain containing 3 (NLRP3) inflammasome. Furthermore, targeting of CIRP by microRNA‑145 or exosome loading with microRNA‑145 attenuated its role in promoting OA both

Indexed as

NF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinOsteoarthritisRNA-Binding ProteinsSignal TransductionToll-Like Receptor 4AnimalsChondrocytesDisease ProgressionExosomesExtracellular MatrixHumansInterleukin-1betaMaleMiceMicroRNAsCIRBP protein, humanInterleukin-1betaMicroRNAsNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanRNA-Binding ProteinsTLR4 protein, humanToll-Like Receptor 4cold‑inducible RNA binding proteinexosomemicroRNA‑145osteoarthritisTLR4/NF‑κB/NLRP3 signaling pathway

Identifiers

PMID41133454
PMCPMC12582850

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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.