ArticleCell biology and toxicology2026
Chronic cadmium exposure promotes TRPM7-dependent acquisition of a myofibroblast-like phenotype in pancreatic stellate cells.
Article in Cell biology and toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. 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
- Erratum issued
Authors and funding
19 authors.
Funding
Abstract
Cadmium (Cd) is a metallic pollutant which has been classified as a possible pancreatic carcinogen. Cd uses similar ion channels than divalent cations to accumulate into the cells. These include the Transient Receptor Potential Cation Channel Subfamily M Member 7 (TRPM7) which has been also shown as a biomarker of pancreatic cancer. Pancreatic carcinogenesis is associated with the establishment of a fibrous stroma induced by pancreatic stellate cell (PSC) activation. Although several stress factors have been identified as activators of PSCs, the impact of pollutants, particularly Cd, is still unknown. Here, we chronically exposed human PSCs to Cd and we observed that Cd-exposed cells acquired a myofibroblast-like phenotype. Moreover, TRPM7 expression and activity were upregulated following Cd exposure. Both TRPM7 inhibition by silencing or NS8593 treatment prevented the Cd-induced PSC cell migration indicating that TRPM7 regulated PSC activation. We used a model of indirect co-culture to study the impact of PSC on MIA PaCa-2 cancer cell migration. Interestingly, we showed that Cd-exposed PSCs stimulated MIA PaCa-2 cancer cell migration to a greater extent than non-exposed PSCs. TRPM7 inhibition in PSCs abolished the migration of cancer cells. Finally, in a mouse model with the KRAS
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.