ArticleACS omega2026
Polystyrene Microplastics Activate Noncanonical TGF‑β Signaling and Metabolomic Reprogramming to Promote Epithelial-Mesenchymal Transition and Fibrosis in the Kidney.
Article in ACS omega, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Micro- and Nanoplastic Pollution and Renal Health: Human Evidence, Mechanisms, and Clinical Implications.Journal of xenobiotics · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polystyrene microplastics (PS-MPs) have been detected in human kidneys, raising concerns about their potential health risks. In this study, we investigated the effects of 1 μm PS-MPs in BALB/c mice and NRK-52E cells. After 28 days of exposure to PS-MPs (0.1, 1, and 10 mg/kg), we observed decreased body weight and elevated levels of serum creatinine and other kidney injury markers. PS-MPs accumulated in the kidney, as confirmed by MicroRaman spectroscopy, and caused significant histopathological changes and an increase in mesenchymal markers (α-SMA, fibronectin, collagen IV, and vimentin) while reducing the epithelial marker, E-Cadherin. Further mechanistic studies revealed the activation of the noncanonical TGFβ pathway involving P38MAPK, Akt, STAT3, STAT5, and NF-κB, which led to epithelial-mesenchymal transition (EMT) and the early onset of kidney fibrosis. Moreover, NMR-based metabolomics indicated changes in metabolites involved in energy and amino-acid metabolism, including decreased levels of branched-chain amino acids (BCAAs; leucine, isoleucine, and valine), phenylalanine, and increased glutamine levels. This altered metabolomic pathways, including the biosynthesis of phenylalanine, tyrosine, and tryptophan, as well as phenylalanine metabolism, which have been previously associated with chronic kidney disease. Overall, this study indicates that exposure to PS-MPs may jeopardize renal health by altering metabolic pathways and signaling related to EMT and kidney fibrosis.
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.