Evidence map›Paper›PMID 33953172›Full record

ArticleCell death & disease2021

Stimulation of α7-nAChRs coordinates autophagy and apoptosis signaling in experimental knee osteoarthritis.

Yuan Liu, Shi Xu, Haijun Zhang, Kaoliang Qian, Jiachen Huang, Xianger Gu, Yan Li, Yi Fan, Jun Hu

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

25 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Article
  3. Early effects of α7nAChR regulation on maxillary expansion in mice : A study on osteogenesis and inflammatory factors.Journal of orofacial orthopedics = Fortschritte der Kieferorthopadie : Organ/official journal Deutsche Gesellschaft fur Kieferorthopadie · 2026
    Article
  4. Article
  5. Ion channels as therapeutic targets in osteoarthritis.Trends in pharmacological sciences · 2025
    Review
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  7. Article
  8. Article
  9. Article
  10. Review
  11. [Activation ofNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Chondrocyte autophagy mechanism and therapeutic prospects in osteoarthritis.Frontiers in cell and developmental biology · 2024
    Review
  17. Article
  18. Article
  19. Article
  20. 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

9 authors at 2 institutions in 1 country.

Yuan Liu *Department of Infectious Diseases, The First Affiliated Hospital of Nanjing Medical University, 210029, Nanjing, China.
Shi Xu *Department of Pharmacology, Nanjing Medical University, 211166, Nanjing, China.
Haijun Zhang *Department of Orthopedics, The First Affiliated Hospital of Nanjing Medical University, 210029, Nanjing, China.
Kaoliang QianDepartment of Orthopedics, The First Affiliated Hospital of Nanjing Medical University, 210029, Nanjing, China.
Jiachen HuangDepartment of Orthopedics, The First Affiliated Hospital of Nanjing Medical University, 210029, Nanjing, China.
Xianger GuDepartment of Pharmacology, Nanjing Medical University, 211166, Nanjing, China.
Yan LiDepartment of Pharmacology, Nanjing Medical University, 211166, Nanjing, China.
Yi FanDepartment of Pharmacology, Nanjing Medical University, 211166, Nanjing, China. Yfan@njmu.edu.cn.ORCID 0000-0003-1783-3220
Jun HuDepartment of Orthopedics, The First Affiliated Hospital of Nanjing Medical University, 210029, Nanjing, China. junhu@njmu.edu.cn.
Jiangsu Province Hospital · CNNanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteoarthritis (OA) is the most common chronic joint disease in the elderly population. Growing evidence indicates that a balance between autophagy and apoptosis in chondrocytes plays a key role in OA's cartilage degradation. Thus, drugs targeting the balance between apoptosis and autophagy are potential therapeutic approaches for OA treatment. In previous studies, we found that the activation of α7 nicotinic acetylcholine receptors (α7-nAChRs) alleviated monosodium iodoacetate (MIA)-induced joint degradation and osteoarthritis pain. To explore the potential functions of α7-nAChRs in autophagy and apoptosis signaling in knee OA, we compared the expression of α7-nAChRs in human knee articular cartilage tissues from normal humans and OA patients. We found that knee joint cartilage tissues of OA patients showed decreased α7-nAChRs and an imbalance between autophagy and apoptosis. Next, we observed that α7-nAChRs deficiency did not affect cartilage degradation in OA development but reversed the beneficial effects of nicotine on mechanical allodynia, cartilage degradation, and an MIA-induced switch from autophagy to apoptosis. Unlike in vivo studies, we found that primary chondrocytes from α7-nAChRs knockout (KO) mice showed decreased LC3 levels under normal conditions and were more sensitive toward MIA-induced apoptosis. Finally, we found that α7-nAChRs deficiency increased the phosphorylation of mTOR after MIA treatment, which can also be observed in OA patients' tissues. Thus, our findings not only confirmed that nicotine alleviated MIA-induced pain behavior and cartilage degradation via stimulating the α7-nAChRs/mTOR signal pathway but found the potential role of α7-nAChRs in mediating the balance between apoptosis and autophagy.

Indexed as

alpha7 Nicotinic Acetylcholine ReceptorAnimalsApoptosisAutophagyDisease Models, AnimalHumansMaleMiceOsteoarthritis, KneeSignal Transductionalpha7 Nicotinic Acetylcholine Receptor

Identifiers

PMID33953172
PMCPMC8100296
OpenAlexW3159695119

What OpenQuestion holds

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LicenceCC BY
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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.