Evidence mapPaperPMID 42233332Full record

ArticleCell transplantation

Mitochondrial transplantation as an immunomodulatory strategy: Modulating polymorphonuclear leukocytes for functional tissue regeneration.

Samantha C Hall, Evan N Main, Gary L Bowlin

Abstract read
In one paragraph

Article in Cell transplantation. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

3 authors.

Samantha C HallDepartment of Biomedical Engineering, The University of Memphis, TN, USA.ORCID 0009-0005-8616-2493
Evan N MainDepartment of Biomedical Engineering, The University of Memphis, TN, USA.ORCID 0000-0001-5527-4939
Gary L BowlinDepartment of Biomedical Engineering, The University of Memphis, TN, USA.ORCID 0000-0003-0917-8203

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Following biomaterial implantation, modulation of the acute immune response is essential for tissue regeneration. Polymorphonuclear leukocytes (PMNs) are critical effector cells in wound healing, and PMN dysfunction is mediated by mitochondrial dysfunction and can lead to prolonged inflammation and tissue damage. It was hypothesized that mitochondrial transplantation could be applied to PMNs in pro-inflammatory states as a means of upregulating regenerative proteins. Primary human PMNs were isolated from donor blood. Isolated PMNs and exogenous mitochondria were co-incubated to induce mitochondrial transplantation. Resulting interactions were assessed through microscopy to confirm initial uptake and mitochondria membrane potential retention, intracellular reactive oxygen species (ROS) analyses (n = 5), and PMN secretome quantification (n = 10) using multiplex protein analysis. Human PMNs were able to successfully uptake delivered mitochondria, and regenerative factors essential for tissue repair and immune cell recruitment including fibroblast growth factor-2 (FGF-2), interleukin (IL)-22, monocyte chemoattractant protein-1 (MCP-1), and granulocyte colony-stimulating factor (G-CSF) were significantly upregulated, indicating that exogenous mitochondria represent promising modulators of PMN function with broad clinical potential.

Indexed as

MitochondriaNeutrophilsRegenerationHumansMembrane Potential, MitochondrialReactive Oxygen SpeciesReactive Oxygen Specieshost-biomaterial responseimmunoengineeringmitochondrial transplantationpolymorphonuclear leukocytetissue regeneration

Identifiers

PMID42233332
PMCPMC13237255

What Socratic holds

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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 Socratic graph.