Evidence map›Paper›PMID 36842089›Full record

ArticleAging2023

Senescence-associated exosomes transfer miRNA-induced fibrosis to neighboring cells.

Amy H Lee, Deepraj Ghosh, Ivy L Koh, Michelle R Dawson

Open access · hybridFull text read
In one paragraph

Article in Aging, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

15 citing papers in PubMed, 12 citations in OpenAlex.

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  11. The impact of cellular senescence on aging skeletal muscle.Frontiers in cell and developmental biology · 2025
    Review
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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

4 authors at 1 institution in 1 country.

Amy H LeeSchool of Engineering, Center for Biomedical Engineering, Brown University, Providence, RI 02912, USA.
Deepraj GhoshMolecular Biology, Cell Biology, and Biochemistry, Brown University, Providence, RI 02912, USA.
Ivy L KohMolecular Biology, Cell Biology, and Biochemistry, Brown University, Providence, RI 02912, USA.
Michelle R DawsonSchool of Engineering, Center for Biomedical Engineering, Brown University, Providence, RI 02912, USA.
Brown University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Radiation-induced fibrosis is a common side effect of radiotherapy, which is the most common treatment for cancer. However, radiation also causes p53-mediated cell cycle arrest, prolonged expression of p21, and the development of senescence in normal cells that reside in irradiated tissues. Bone marrow-derived mesenchymal stem cells (MSCs) accumulate in primary tumor sites because of their natural tropism for inflammatory and fibrotic tissues. MSCs are extremely sensitive to low doses of ionizing radiation and acquire senescence as a result of bystander radiation effects. Senescent cells remain metabolically active but develop a potent senescence-associated secretory phenotype (SASP) that correlates to hyperactive secretion of cytokines, pro-fibrotic growth factors, and exosomes (EXOs). Integrative pathway analysis highlighted that radiation-induced senescence significantly enriched cell-cycle, extracellular matrix, transforming growth factor-β (TGF-β) signaling, and vesicle-mediated transport genes in MSCs. EXOs are cell-secreted nanovesicles (a subclass of small extracellular vesicles) that contain biomaterials-proteins, RNAs, microRNAs (miRNAs)-that are critical in cell-cell communication. miRNA content analysis of secreted EXOs further revealed that radiation-induced senescence uniquely altered miRNA profiles. In fact, several of the standout miRNAs directly targeted TGF-β or downstream genes. To examine bystander effects of radiation-induced senescence, we further treated normal MSCs with senescence-associated EXOs (SA-EXOs). These modulated genes related to TGF-β pathway and elevated both alpha smooth muscle actin (protein increased in senescent, activated cells) and Ki-67 (proliferative marker) expression in SA-EXO treated MSCs compared to untreated MSCs. We revealed SA-EXOs possess unique miRNA content that influence myofibroblast phenotypes via TGF-β pathway activation. This highlights that SA-EXOs are potent SASP factors that play a large role in cancer-related fibrosis.

Indexed as

ExosomesExtracellular VesiclesMicroRNAsFibrosisHumansTransforming Growth Factor betaMicroRNAsTransforming Growth Factor betaexosomes (EXOs)mesenchymal stem cells (MSCs)microRNA (miRNA)radiation-induced senescencetransforming growth factor-β (TGF-β)

Identifiers

PMID36842089
PMCPMC10042705
OpenAlexW4321617869

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read39
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.