Evidence map›Paper›PMID 42011979›Full record

ReviewClinical and translational medicine2026

Leveraging extracellular vesicle biology for novel tests and therapeutics for kidney fibrosis.

Chin-Ya Sophie Chiang, Andrew J Kassianos, Helen Grania Healy, Monica Suet Ying Ng

Abstract readReview
In one paragraph

Review in Clinical and translational medicine, 2026. 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

4 authors.

Chin-Ya Sophie ChiangKidney Health Service, Royal Brisbane and Women's Hospital, Herston, Queensland, Australia.ORCID 0009-0002-6571-2191
Andrew J KassianosKidney Health Service, Royal Brisbane and Women's Hospital, Herston, Queensland, Australia.ORCID 0000-0002-0994-3588
Helen Grania HealyKidney Health Service, Royal Brisbane and Women's Hospital, Herston, Queensland, Australia.ORCID 0000-0003-4342-5300
Monica Suet Ying NgKidney Health Service, Royal Brisbane and Women's Hospital, Herston, Queensland, Australia.ORCID 0000-0002-0431-9110

Funding

Health Innovation, Investment and Research Office: Queensland Health Clinical Research FellowshipMetro North Hospital and Health Service CRF-606-2024Royal Australasian College of Physicians 2025REF008
6 · The paper itself

Abstract

Kidney fibrosis is mechanistically characterised by tissue injury followed by development of a fibrogenic niche. The fibrogenic niche involves chronic inflammation, vascular rarefaction, glomerulosclerosis, tubular atrophy, interstitial accumulation of extracellular matrix which replaces functional kidney parenchyma-culminating in reduced kidney function. Extracellular vesicles are bilipid membrane-encased nanoparticles that play critical roles as cell-to-cell messengers and waste management mechanisms. Extracellular vesciels communication has been demonstrated within the glomerulus, within the tubular compartment and, between tubular and glomerular compartments. Diverse extracellular vesicle cargoes interact with key pathways regulating cell facte and inflammation to mediate kidney fibrosis. Extracellular vesicles cargos can be leveraged as biomarkers to develop minimally invasive tests for kidney fibrosis and pinpoint active pathobiological processes to guide personalised mechanism-driven care. Mesechymal cell-derived extracellular vesicles, extracellular vesicles from bioengineered cells, post-modified extracellular vesicles and suppression of extracellular vesicle uptake have demonstrated promise in preclinical studies for preventing kidney fibrosis. Roadblocks to clinical implementation of extracellular vesicles as biomarkers include lack of standardised collection, measurement, normalisation and data processing protocols; as well as dearth of highly specific biomaker panels. Roadblocks to extracellular vesicle therapeutics include extracellular vesicle heterogeneity, sensitivity to small changes in production parameters, absence of standardised characterisation protocols, technological limitations and knowledge gaps on extracellular vesicle mechanisms of action. This review will contextualise kidney extracellular vesicle pathobiology with principles of clinical implementation to highlight extracellular vesicle potential as minimally invasive biomarkers and novel therapeutics for kidney fibrosis. Strategies to address roadblocks to clinical implementation of extracellular vesicles for kidney fibrosis and chronic kidney disease management will also be explored in this review. KEY POINTS: Extracellular vesicles (EVs) are bilipid membrane-encased nanoparticles that play critical roles as cell-to-cell messengers and waste management mechanisms. EV cargos can be leveraged as biomarkers to develop minimally invasive tests for kidney fibrosis and guide personalised mechanism-driven care. Mesenchymal cell-derived EVs, EVs from bioengineered cells, post-modified EVs and suppression of EV uptake have demonstrated promise for preventing kidney fibrosis.

Indexed as

Extracellular VesiclesFibrosisKidneyKidney DiseasesAnimalsBiomarkersHumansBiomarkersbiomarkersextracellular vesicleskidney fibrosistherapeutics

Identifiers

PMID42011979
PMCPMC13097387

What Socratic holds

Textmetadata
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 Socratic graph.