ReviewInternational journal of molecular medicine2025
Developments in the connection between epithelial‑mesenchymal transition and endoplasmic reticulum stress (Review).
Review in International journal of molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed.
- ZBTB11 Promotes Breast Cancer Progression by Activating FBXO28-Mediated MST1 Degradation and Suppressing Hippo Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Advances regarding the mechanism of endoplasmic reticulum stress in diabetic kidney disease and pharmacological interventions (Review).Molecular medicine reports · 2026Review
- Airway remodeling in chronic obstructive pulmonary disease: characteristics and opportunities.Frontiers in medicine · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endoplasmic reticulum stress (ERS) and epithelial‑mesenchymal transition (EMT) have important roles in fibrosis and tumour development. Moderate ERS activates cellular defence mechanisms in response to noxious stimuli; however, sustained or overly strong ERS induces apoptosis. In this disease process, EMT induces epithelial cells to acquire the ability to migrate and invade. Reportedly, ERS directly or indirectly regulates EMT processes through multiple mechanisms (such as key transcription factors, signalling pathways, ferroptosis, autophagy and oxidative stress), and both processes form a complex network of interactions. Given the critical roles of ERS and EMT in disease, targeted intervention of these two processes has emerged as a potential therapeutic strategy. In the present study, the molecular interaction mechanism of ERS and EMT was systematically explored, research progress in fibrotic and neoplastic diseases was reviewed and the potential application prospects of related targeted therapies were examined, which may provide new ideas for the development of drugs to reverse fibrosis and treat tumours.
Indexed as
Identifiers
What Socratic 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 Socratic graph.