Evidence map›Paper›PMID 33808727›Full record

ArticleCells2021

Metformin Attenuates Monosodium-Iodoacetate-Induced Osteoarthritis via Regulation of Pain Mediators and the Autophagy-Lysosomal Pathway.

Hyun Sik Na, Ji Ye Kwon, Seon-Yeong Lee, Seung Hoon Lee, A Ram Lee, Jin Seok Woo, KyungAh Jung, Keun-Hyung Cho, Jeong-Won Choi, Dong Hwan Lee and 4 more

Open access · goldFull text read
In one paragraph

Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
8.0field-weighted citation impact, top 2% 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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
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  5. Article
  6. Article
  7. Article
  8. Review
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  10. Article
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  12. Article
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  14. Article
  15. Metformin and bone metabolism: unraveling their direct and indirect effects.Therapeutic advances in endocrinology and metabolism · 2025
    Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Chondrocyte autophagy mechanism and therapeutic prospects in osteoarthritis.Frontiers in cell and developmental biology · 2024
    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

14 authors at 4 institutions in 1 country.

Hyun Sik NaThe Rheumatism Research Center, Catholic Reasearch Institute of Medical Science, The Catholic University of Korea, Seoul 06591, Korea.
Ji Ye KwonThe Rheumatism Research Center, Catholic Reasearch Institute of Medical Science, The Catholic University of Korea, Seoul 06591, Korea.
Seon-Yeong LeeThe Rheumatism Research Center, Catholic Reasearch Institute of Medical Science, The Catholic University of Korea, Seoul 06591, Korea.
Seung Hoon LeeThe Rheumatism Research Center, Catholic Reasearch Institute of Medical Science, The Catholic University of Korea, Seoul 06591, Korea.
A Ram LeeThe Rheumatism Research Center, Catholic Reasearch Institute of Medical Science, The Catholic University of Korea, Seoul 06591, Korea.
Jin Seok WooThe Rheumatism Research Center, Catholic Reasearch Institute of Medical Science, The Catholic University of Korea, Seoul 06591, Korea.ORCID 0000-0001-8921-2832
KyungAh JungImpact Biotech, Korea 505 Banpo-Dong, Seocho-Ku, Seoul 06591, Korea.
Keun-Hyung ChoThe Rheumatism Research Center, Catholic Reasearch Institute of Medical Science, The Catholic University of Korea, Seoul 06591, Korea.
Jeong-Won ChoiThe Rheumatism Research Center, Catholic Reasearch Institute of Medical Science, The Catholic University of Korea, Seoul 06591, Korea.
Dong Hwan LeeDepartment of Orthopedic Surgery, Uijeongbu St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul 11765, Korea.ORCID 0000-0002-7798-5894
Hong-Ki MinDivision of Rheumatology, Department of Internal Medicine, Konkuk University Medical Center, Seoul 05030, Korea.ORCID 0000-0003-1147-1046
Sung-Hwan ParkDivision of Rheumatology, Department of Internal Medicine, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul 06591, Korea.
Seok Jung KimDepartment of Orthopedic Surgery, Uijeongbu St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul 11765, Korea.ORCID 0000-0002-9116-8786
Mi-La ChoThe Rheumatism Research Center, Catholic Reasearch Institute of Medical Science, The Catholic University of Korea, Seoul 06591, Korea.
Catholic University of Korea · KRThe Catholic University of Korea Uijeongbu St. Mary's Hospital · KRKonkuk University Medical Center · KRThe Catholic University of Korea Seoul St. Mary's Hospital · KR

Funding

Bio & Medical Technology Development Program of the National Research Foundation (NRF) funded by the Korean government (MSIT) NRF-2017M3A9B4028022National Research Foundation of Korea (NRF) grant funded by the Korea government (MSIP) NRF-2017R1A2B3007688
6 · The paper itself

Abstract

Osteoarthritis (OA) is the most common degenerative arthritis associated with pain and cartilage destruction in the elderly; it is known to be involved in inflammation as well. A drug called celecoxib is commonly used in patients with osteoarthritis to control pain. Metformin is used to treat type 2 diabetes but also exhibits regulation of the autophagy pathway. The purpose of this study is to investigate whether metformin can treat monosodium iodoacetate (MIA)-induced OA in rats. Metformin was administered orally every day to rats with OA. Paw-withdrawal latency and threshold were used to assess pain severity. Cartilage damage and pain mediators in dorsal root ganglia were evaluated by histological analysis and a scoring system. Relative mRNA expression was measured by real-time PCR. Metformin reduced the progression of experimental OA and showed both antinociceptive properties and cartilage protection. The combined administration of metformin and celecoxib controlled cartilage damage more effectively than metformin alone. In chondrocytes from OA patients, metformin reduced catabolic factor gene expression and inflammatory cell death factor expression, increased LC3Ⅱb, p62, and LAMP1 expression, and induced an autophagy-lysosome fusion phenotype. We investigated if metformin treatment reduces cartilage damage and inflammatory cell death of chondrocytes. The results suggest the potential for the therapeutic use of metformin in OA patients based on its ability to suppress pain and protect cartilage.

Indexed as

AnimalsArthritis, ExperimentalCelecoxibChondrocytesDiabetes Mellitus, Type 2Disease Models, AnimalIodoacetatesLysosomesMetforminOsteoarthritisPainRatsRats, WistarCelecoxibIodoacetatesMetforminautophagycartilagecombination therapymetforminosteoarthritispain

Identifiers

PMID33808727
PMCPMC8003384
OpenAlexW3137973154

What OpenQuestion holds

Textfull text, public
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.