Evidence map›Paper›PMID 35573148›Full record

ArticleImmune network2022

Mitochondrial Transplantation Ameliorates the Development and Progression of Osteoarthritis.

A Ram Lee, Jin Seok Woo, Seon-Yeong Lee, Hyun Sik Na, Keun-Hyung Cho, Yeon Su Lee, Jeong Su Lee, Seon Ae Kim, Sung-Hwan Park, Seok Jung Kim and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Immune network, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
9.2field-weighted citation impact, top 1% 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

31 citing papers in PubMed, 56 citations in OpenAlex.

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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.

A Ram LeeRheumatism Research Center, College of Medicine, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul 06591, Korea.
Jin Seok WooRheumatism Research Center, College of Medicine, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul 06591, Korea.ORCID https://orcid.org/0000-0001-8921-2832
Seon-Yeong LeeRheumatism Research Center, College of Medicine, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul 06591, Korea.
Hyun Sik NaRheumatism Research Center, College of Medicine, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul 06591, Korea.
Keun-Hyung ChoRheumatism Research Center, College of Medicine, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul 06591, Korea.
Yeon Su LeeRheumatism Research Center, College of Medicine, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul 06591, Korea.
Jeong Su LeeRheumatism Research Center, College of Medicine, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul 06591, Korea.
Seon Ae KimDepartment of Orthopedic Surgery, College of Medicine, The Catholic University of Korea, Seoul 06591, Korea.
Sung-Hwan ParkRheumatism Research Center, College of Medicine, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul 06591, Korea.
Seok Jung KimDepartment of Orthopedic Surgery, College of Medicine, The Catholic University of Korea, Seoul 06591, Korea.
Mi-La ChoRheumatism Research Center, College of Medicine, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul 06591, Korea.ORCID https://orcid.org/0000-0001-5715-3989
Catholic University of Korea · KRThe Catholic University of Korea Seoul St. Mary's Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteoarthritis (OA) is a common degenerative joint disease characterized by breakdown of joint cartilage. Mitochondrial dysfunction of the chondrocyte is a risk factor for OA progression. We examined the therapeutic potential of mitochondrial transplantation for OA. Mitochondria were injected into the knee joint of monosodium iodoacetate-induced OA rats. Chondrocytes from OA rats or patients with OA were cultured to examine mitochondrial function in cellular pathophysiology. Pain, cartilage destruction, and bone loss were improved in mitochondrial transplanted-OA rats. The transcript levels of IL-1β, TNF-α, matrix metallopeptidase 13, and MCP-1 in cartilage were markedly decreased by mitochondrial transplantation. Mitochondrial function, as indicated by membrane potential and oxygen consumption rate, in chondrocytes from OA rats was improved by mitochondrial transplantation. Likewise, the mitochondrial function of chondrocytes from OA patients was improved by coculture with mitochondria. Furthermore, inflammatory cell death was significantly decreased by coculture with mitochondria. Mitochondrial transplantation ameliorated OA progression, which is caused by mitochondrial dysfunction. These results suggest the therapeutic potential of mitochondrial transplantation for OA.

Indexed as

AutophagyMitochondrial dysfunctionMitochondrial transplantationNecroptosisOsteoarthritis

Identifiers

PMID35573148
PMCPMC9066007
OpenAlexW4280584125

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.