The global burden of chronic liver disease is rising along a well-defined trajectory—from simple steatosis to metabolic dysfunction-associated steatotic liver disease (MASLD), metabolic dysfunction-associated steatohepatitis (MASH), fibrosis, and ultimately hepatocellular carcinoma (HCC)—yet genetics and lifestyle alone cannot account for this trend. Environmental exposures are increasingly implicated as drivers of disease onset and progression along this continuum, and as modifiers of susceptibility and severity in alcohol-associated liver disease (ALD). A critical gap remains in understanding how pervasive agents such as endocrine-disrupting chemicals, air pollutants, dietary additives, and microplastics interact—individually and as mixtures—with metabolic and hepatic pathways to accelerate steatosis, inflammation, fibrosis, and malignant transformation. Because most people are exposed to complex combinations of environmental agents rather than single compounds, understanding cumulative exposome burden and individual susceptibility is essential to explaining why disease trajectories vary so widely between individuals.
This Research Topic consolidates research using exposomics, multi-omics, and novel model systems to map the environmental-molecular pathways underlying liver disease progression. We aim to identify sensitive exposure biomarkers, clarify how exposure mixtures and cumulative burden modify individual risk, and integrate environmental data into predictive risk models—translating mechanistic insight into hepatoprotective and preventive strategies for an exposome-aware approach to hepatology.
We welcome original research, reviews, and perspectives addressing, but not limited to:
- Environmental exposures and disease progression: How endocrine disruptors, microplastics, heavy metals, air pollutants, and dietary additives—alone or as exposure mixtures—influence the trajectory from steatosis through MASLD, MASH, fibrosis, and HCC, and how they modulate susceptibility and severity in ALD. Contributions on microplastics are encouraged, with causal claims calibrated to current levels of evidence given the still-emerging nature of this literature.
- Molecular mechanisms: Oxidative stress, endoplasmic reticulum stress, epigenetic modification, and gut-liver axis dysregulation as mediators linking environmental insults to hepatic injury and disease progression.
- Exposure complexity and individual susceptibility: Methodologies and findings addressing cumulative exposome burden, mixture effects, and genetic or metabolic factors that determine why comparable exposures produce divergent disease outcomes.
- Biomarkers and prevention: Exposomics, metabolomics, transcriptomics, and spatial omics approaches to identify exposure biomarkers for early detection and risk stratification; preclinical models recapitulating environmental insults; and translational strategies for personalized prevention and hepatoprotection.
We encourage interdisciplinary contributions bridging environmental science, toxicology, immunology, and clinical hepatology to advance actionable, exposome-informed strategies across the full continuum of liver disease.
Article types and fees
This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:
Brief Research Report
Case Report
Classification
Clinical Trial
Community Case Study
Curriculum, Instruction, and Pedagogy
Data Report
Editorial
FAIR² Data
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Article types
This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:
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