Evidence map›Paper›PMID 33677475›Full record

ArticleActa biochimica et biophysica Sinica2021

Interleukin 1 beta-induced chloride currents are important in osteoarthritis onset: an in vitro study.

Zhiqin Deng, Zicong Lin, Qing Zhong, Minqiang Lu, Huankun Fang, Jianquan Liu, Li Duan, Lixin Chen, Liwei Wang, Daping Wang and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Acta biochimica et biophysica Sinica, 2021. 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
2.6field-weighted citation impact, top 11% 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. Ion channels as therapeutic targets in osteoarthritis.Trends in pharmacological sciences · 2025
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  10. The Mechanism of Bone Remodeling After Bone Aging.Clinical interventions in aging · 2022
    Review
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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

11 authors at 2 institutions in 1 country.

Zhiqin DengGuangdong Provincial Research Center for Artificial Intelligence and Digital Orthopedic Technology, Hand and Foot Surgery Department, Shenzhen Second People's Hospital (The First Hospital Affiliated to Shenzhen University), Shenzhen 518000, China.
Zicong LinGuangdong Provincial Research Center for Artificial Intelligence and Digital Orthopedic Technology, Hand and Foot Surgery Department, Shenzhen Second People's Hospital (The First Hospital Affiliated to Shenzhen University), Shenzhen 518000, China.
Qing ZhongGuangdong Provincial Research Center for Artificial Intelligence and Digital Orthopedic Technology, Hand and Foot Surgery Department, Shenzhen Second People's Hospital (The First Hospital Affiliated to Shenzhen University), Shenzhen 518000, China.
Minqiang LuGuangdong Provincial Research Center for Artificial Intelligence and Digital Orthopedic Technology, Hand and Foot Surgery Department, Shenzhen Second People's Hospital (The First Hospital Affiliated to Shenzhen University), Shenzhen 518000, China.
Huankun FangGuangdong Provincial Research Center for Artificial Intelligence and Digital Orthopedic Technology, Hand and Foot Surgery Department, Shenzhen Second People's Hospital (The First Hospital Affiliated to Shenzhen University), Shenzhen 518000, China.
Jianquan LiuGuangdong Provincial Research Center for Artificial Intelligence and Digital Orthopedic Technology, Hand and Foot Surgery Department, Shenzhen Second People's Hospital (The First Hospital Affiliated to Shenzhen University), Shenzhen 518000, China.
Li DuanGuangdong Provincial Research Center for Artificial Intelligence and Digital Orthopedic Technology, Hand and Foot Surgery Department, Shenzhen Second People's Hospital (The First Hospital Affiliated to Shenzhen University), Shenzhen 518000, China.
Lixin ChenDepartment of Pharmacology, Medical College, Jinan University, Guangzhou 510632, China.
Liwei WangDepartment of Physiology, Medical College, Jinan University, Guangzhou 510632, China.
Daping WangGuangdong Provincial Research Center for Artificial Intelligence and Digital Orthopedic Technology, Hand and Foot Surgery Department, Shenzhen Second People's Hospital (The First Hospital Affiliated to Shenzhen University), Shenzhen 518000, China.
Wencui LiGuangdong Provincial Research Center for Artificial Intelligence and Digital Orthopedic Technology, Hand and Foot Surgery Department, Shenzhen Second People's Hospital (The First Hospital Affiliated to Shenzhen University), Shenzhen 518000, China.
Shenzhen Second People's Hospital · CNJinan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Persistent hypotonic and inflammatory conditions in the joint cavity can lead to the loss of cartilage matrix and cell death, which are the important mechanisms of osteoarthritis (OA) onset. Previous studies have confirmed that the existence of a hypotonic environment is a red flag for inflammation, as hypotonic environment induces the opening of the chloride channel of the cell and promotes chloride ion efflux, which prompts the cell volume to increase. Chloride channels play an important role in the regulation of mineralization and chondrocyte death. Here, we reported that OA chondrocytes showed a significant increase of cell death rate and the imbalance of cartilage matrix catabolism. We found that the distribution of skeleton protein F-actin was disordered. In addition, the volume-sensitive chloride current of OA chondrocytes decreased significantly with the increase of the expression levels of inflammation-related proteins caspase-1, caspase-3, and NLRP3. Moreover, interleukin-1β (IL-1β) showed a potential to activate the chloride current of normal chondrocytes. These results indicate that IL-1β-induced chloride channel opening in chondrocytes may be closely related to the occurrence of OA. This chloride channel opening process may therefore be a potential target for the treatment of OA.

Indexed as

AgedAged, 80 and overChloridesChondrocytesFemaleHumansInflammationInterleukin-1betaIon TransportMaleOsteoarthritisChloridesIL1B protein, humanInterleukin-1betachloride channelhypotonicIL-1βinflammationosteoarthritis

Identifiers

PMID33677475
PMCPMC7996641
OpenAlexW3133787635

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.