ReviewAnnals of medicine2025
Clock genes in pancreatic disease progression: from circadian regulation to dysfunction.
Review in Annals of medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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
6 citing papers in PubMed.
- Night shift work and risk of total and site-specific cancer: results from a prospective cohort study among Chinese men.Scandinavian journal of work, environment & health · 2026Article
- D-Box Binding Protein (DBP) as a Circadian Output Regulator: Molecular Mechanisms, Tissue-Specific Functions, and Disease Relevance.International journal of molecular sciences · 2026Review
- Immunohistochemical expression of pancreatic melatonin receptor (MTNR1B) under experimental sleep disturbance in rats.Journal of molecular histology · 2026Article
- Global surge in pancreatic cancer cases driven by ageing populations and modifiable risks.Journal of global health · 2026Article
- Immune Checkpoint Restoration as a Therapeutic Strategy to Halt Diabetes-Driven Atherosclerosis.Biology · 2025Review
- Cross-tissue transcriptome-wide association identify novel T1D susceptibility genes and drug candidates.Frontiers in immunology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCircadian rhythms, governed by core clock genes, are essential for maintaining metabolic, endocrine, and immune homeostasis. Disruption of these rhythms has been increasingly implicated in the pathogenesis of various pancreatic diseases.
objectiveThis review summarizes current evidence on the role of circadian rhythm disruption in pancreatic diseases, including type 2 diabetes (T2D), type 1 diabetes (T1D), pancreatitis, and pancreatic cancer (PC), with a focus on underlying mechanisms involving clock gene dysregulation. RECENT
findingsIn T2D, dampened oscillations of clock gene expression in pancreatic islets are associated with impaired insulin secretion and loss of cellular synchrony. In T1D, circadian dysregulation enhances immune activation and reduces β-cell tolerance, accelerating disease progression. In pancreatitis, especially in chronic forms, loss of core clock components such as Bmal1 exacerbates pancreatic stellate cell activation, fibrosis, and inflammatory cytokine release. Additionally, circadian disruption has been linked to pancreatic tumorigenesis, suggesting a potential role of clock genes in early cancer development through modulation of the inflammatory microenvironment and stromal remodeling.
conclusionCircadian clock genes play a multifaceted role in pancreatic disease pathophysiology, extending beyond metabolic regulation to influence immune responses, inflammation, and tumorigenesis. Understanding these mechanisms may inform the development of novel circadian-based therapeutic strategies for pancreatic disorders.
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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.