Evidence map›Paper›PMID 35230643›Full record

ArticleStem cell reviews and reports2022

Artificial Mitochondrial Transfer (AMT) for the Management of Age-related Musculoskeletal Degenerative Disorders: An Emerging Avenue for Bone and Cartilage Metabolism Regulation.

Lynda Bourebaba, Katarzyna Kornicka-Garbowska, Larry Galuppo, Krzysztof Marycz

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Article in Stem cell reviews and reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 34% 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

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
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  4. 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

4 authors at 2 institutions in 2 countries.

Lynda BourebabaDepartment of Experimental Biology, Faculty of Biology and Animal Science, Wrocław University of Environmental and Life Sciences, Norwida 27B, 50-375, Wrocław, Poland.
Katarzyna Kornicka-GarbowskaDepartment of Experimental Biology, Faculty of Biology and Animal Science, Wrocław University of Environmental and Life Sciences, Norwida 27B, 50-375, Wrocław, Poland.
Larry GaluppoDepartment of Surgical and Radiological Sciences, School of Veterinary Medicine, University of California, Davis, Davis, CA, 95516, USA.
Krzysztof MaryczDepartment of Experimental Biology, Faculty of Biology and Animal Science, Wrocław University of Environmental and Life Sciences, Norwida 27B, 50-375, Wrocław, Poland. kmmarycz@ucdavis.edu.ORCID 0000-0003-3676-796X
Wrocław University of Environmental and Life Sciences · PLUniversity of California, Davis · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Musculoskeletal system disorders are among the most common age-related conditions worldwide. All associated with a degeneration of the supporting tissues under pro-inflammatory micro- and macro-environments, the erosion of cartilage and later of bones, are the main hallmarks of these pathologies. Affected chondrocytes, osteoblasts and synoviocytes, that are all critical actors in the bone and cartilage defects exhibit mitochondrial dysfunction that develops immediately following cartilage and bone injury, and leads to tissue residing specific cell death, cartilage degeneration, bone erosion, and ultimately post-traumatic musculoskeletal degeneration. Herein, we would like to introduce a novel concept for bone and cartilage related defects treatment based on artificial transfer of exogeneous functional mitochondria (AMT). Particularly, we believe that because mitochondrial failure critically contributes to degenerative disorders onset and progression, replacing malfunctioning mitochondria with their healthy and functional counterparts can represent a novel, and effective therapeutic solution for the management of bone and cartilage related degenerative diseases. Artificial mitochondrial transfer (AMT) may reverse the failed metabolic status of musculoskeletal tissues cells and reduce bone and cartilage tissues defects by restoring mitochondrial bioenergetics.

Indexed as

Cartilage, ArticularCartilage DiseasesBone and BonesChondrocytesHumansMitochondriaAgingATMBone defectMitochondrial DysfunctionOXPHOSSynovitis

Identifiers

PMID35230643
OpenAlexW4214680074

What OpenQuestion holds

Textmetadata
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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.