Evidence map›Paper›PMID 33925007›Full record

ArticleAntioxidants (Basel, Switzerland)2021

Mitochondrial Transplantation Modulates Inflammation and Apoptosis, Alleviating Tendinopathy Both In Vivo and In Vitro.

Ji Min Lee, Jung Wook Hwang, Mi Jin Kim, Sang Youn Jung, Kyung-Soo Kim, Eun Hee Ahn, Kyunghoon Min, Yong-Soo Choi

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
13.1field-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

52 citing papers in PubMed, 97 citations in OpenAlex.

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  5. Methylene blue restores NADJournal of orthopaedic translation · 2026
    Article
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  7. Therapeutic Potential of Mitochondrial Transplantation with Focus on DBD.International journal of molecular sciences · 2026
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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

8 authors at 2 institutions in 1 country.

Ji Min LeeDepartment of Biotechnology, CHA University, Seongnam 13488, Korea.
Jung Wook HwangDepartment of Biotechnology, CHA University, Seongnam 13488, Korea.
Mi Jin KimDepartment of Biotechnology, CHA University, Seongnam 13488, Korea.ORCID 0000-0002-0594-5703
Sang Youn JungDivision of Rheumatology, Department of Internal Medicine, CHA Bundang Medical Center, CHA University School of Medicine, Seongnam 13496, Korea.
Kyung-Soo KimDivision of Endocrinology and Metabolism, Department of Internal Medicine, CHA Bundang Medical Center, CHA University School of Medicine, Seongnam 13496, Korea.
Eun Hee AhnDepartment of Obstetrics & Gynecology, CHA Bundang Medical Center, CHA University School of Medicine, Seongnam 13496, Korea.
Kyunghoon MinDepartment of Rehabilitation Medicine, CHA Bundang Medical Center, CHA University School of Medicine, Seongnam 13496, Korea.ORCID 0000-0003-3357-9795
Yong-Soo ChoiDepartment of Biotechnology, CHA University, Seongnam 13488, Korea.
CHA University · KRCHA University Bundang Medical Center · KR

Funding

National Research Foundation of Korea (NRF) grant funded by the Korean government (MSIP), Bio & Medical Technology Development Program of the National Research Foundation of Korea (NRF) funded by the Ministry of Science and ICT 2020R1F1A1048532, NRF-2018M3A9B5023052
6 · The paper itself

Abstract

Tendinopathy is a common musculoskeletal condition causing pain and dysfunction. Conventional treatment and surgical procedures for tendinopathy are insufficient; accordingly, recent research has focused on tendon-healing regenerative approaches. Tendon injuries usually occur in the hypoxic critical zone, characterized by increased oxidative stress and mitochondrial dysfunction; thus, exogenous intact mitochondria may be therapeutic. We aimed to assess whether mitochondrial transplantation could induce anti-inflammatory activity and modulate the metabolic state of a tendinopathy model. Exogenous mitochondria were successfully delivered into damaged tenocytes by centrifugation. Levels of Tenomodulin and Collagen I in damaged tenocytes were restored with reductions in nuclear factor-κB and matrix metalloproteinase 1. The dysregulation of oxidative stress and mitochondrial membrane potential was attenuated by mitochondrial transplantation. Activated mitochondrial fission markers, such as fission 1 and dynamin-related protein 1, were dose-dependently downregulated. Apoptosis signaling pathway proteins were restored to the pre-damage levels. Similar changes were observed in a collagenase injection-induced rat model of tendinopathy. Exogenous mitochondria incorporated into the Achilles tendon reduced inflammatory and fission marker levels. Notably, collagen production was restored. Our results demonstrate the therapeutic effects of direct mitochondrial transplantation in tendinopathy. These effects may be explained by alterations in anti-inflammatory and apoptotic processes via changes in mitochondrial dynamics.

Indexed as

apoptosisinflammationmitochondrial dynamicsmitochondrial transplantationtendinopathytenocyte

Identifiers

PMID33925007
PMCPMC8146308
OpenAlexW3158922010

What OpenQuestion holds

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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.