Evidence map›Paper›PMID 36513773›Full record

ArticleScientific reports2022

Mesenchymal stromal cells donate mitochondria to articular chondrocytes exposed to mitochondrial, environmental, and mechanical stress.

Megan Fahey, Maureen Bennett, Matthew Thomas, Kaylee Montney, Irene Vivancos-Koopman, Brenna Pugliese, Lindsay Browning, Lawrence J Bonassar, Michelle Delco

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

28 citing papers in PubMed, 33 citations in OpenAlex.

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  4. Building the bridges: molecular mechanisms of tunneling nanotube formation.Cellular and molecular life sciences : CMLS · 2026
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  8. Mitochondria transfer in tissue homeostasis and diseases.International journal of biological 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

9 authors at 1 institution in 1 country.

Megan Fahey *Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY, 14853, USA.
Maureen Bennett *Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY, 14853, USA.
Matthew ThomasDepartment of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY, 14853, USA.
Kaylee MontneyDepartment of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY, 14853, USA.
Irene Vivancos-KoopmanDepartment of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY, 14853, USA.
Brenna PuglieseDepartment of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY, 14853, USA.
Lindsay BrowningMeinig School of Biomedical Engineering, Sibley School of Mechanical and Aerospace Engineering, Cornell University, Ithaca, NY, 14853, USA.
Lawrence J BonassarMeinig School of Biomedical Engineering, Sibley School of Mechanical and Aerospace Engineering, Cornell University, Ithaca, NY, 14853, USA.
Michelle DelcoDepartment of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY, 14853, USA. mld12@cornell.edu.
Cornell University · US

Funding

Mitochondrial dysfunction as a link between cartilage injury and osteoarthritisK08AR068470 · NIAMS · CORNELL UNIVERSITY · PI DELCO, MICHELLE LEE · 2016 to 2021
$724k
The role of mitochondrial Damage Associated Molecular Patterns (mDAMPs) in posttraumatic osteoarthritis.R03AR075929 · NIAMS · CORNELL UNIVERSITY · PI DELCO, MICHELLE LEE · 2019 to 2020
$157k
NIAMS NIH HHS K08 AR068470NIAMS NIH HHS R03 AR075929
6 · The paper itself

Abstract

Articular cartilage has limited healing capacity and no drugs are available that can prevent or slow the development of osteoarthritis (OA) after joint injury. Mesenchymal stromal cell (MSC)-based regenerative therapies for OA are increasingly common, but questions regarding their mechanisms of action remain. Our group recently reported that although cartilage is avascular and relatively metabolically quiescent, injury induces chondrocyte mitochondrial dysfunction, driving cartilage degradation and OA. MSCs are known to rescue injured cells and improve healing by donating healthy mitochondria in highly metabolic tissues, but mitochondrial transfer has not been investigated in cartilage. Here, we demonstrate that MSCs transfer mitochondria to stressed chondrocytes in cell culture and in injured cartilage tissue. Conditions known to induce chondrocyte mitochondrial dysfunction, including stimulation with rotenone/antimycin and hyperoxia, increased transfer. MSC-chondrocyte mitochondrial transfer was blocked by non-specific and specific (connexin-43) gap-junction inhibition. When exposed to mechanically injured cartilage, MSCs localized to areas of matrix damage and extended cellular processes deep into microcracks, delivering mitochondria to chondrocytes. This work provides insights into the chemical, environmental, and mechanical conditions that can elicit MSC-chondrocyte mitochondrial transfer in vitro and in situ, and our findings suggest a new potential role for MSC-based therapeutics after cartilage injury.

Indexed as

Cartilage, ArticularMesenchymal Stem CellsOsteoarthritisChondrocytesHumansMitochondriaStress, Mechanical

Identifiers

PMID36513773
PMCPMC9747781
OpenAlexW4311362286

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.