ArticleFrontiers in physiology2026
A comprehensive approach to elucidating the pathophysiology of kidney fibrosis based on extracellular vesicle proteomics.
Article in Frontiers in physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Transglutaminase 2 (TG2) plays a profibrotic role in chronic kidney disease (CKD), but its role in the exosomal proteome remains unexplored. Here, we aimed to evaluate biological processes specifically involved in CKD progression through exosomal proteomic profiling following TG2 inhibition. Materials and methods: Human proximal tubular epithelial cells (hPTECs) were treated with recombinant transforming growth factor-β (rTGF-β) to induce fibrosis and cysteamine to inhibit TG2. A unilateral ureteral obstruction (UUO) mouse model was used for Results: TG2 inhibition attenuated the expression of fibrosis- and inflammation-associated proteins in hPTECs and fibroblasts. EV proteomic analysis revealed distinct protein expression patterns following rTGF-β treatment and TG2 inhibition. Altered proteins were primarily extracellular matrix components such as connective tissue growth factor, IGF-binding protein, laminin, plasminogen activator inhibitor, periostin, and collagen. Conclusions: TG2 inhibition modulated EV-associated proteins involved in fibrosis and inflammation, highlighting its therapeutic potential in CKD. Identifying reversible fibrosis-related factors may provide new targets for CKD treatment.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.