Inflammation and Fibrosis in the Gastrointestinal Tract and Liver, Volume II

Building on the strong foundation laid by Volume I, this Research Topic returns to inflammation and fibrosis of the gastrointestinal tract and liver at a pivotal moment for the field. Since the publication of Volume I, new disease classifications have been adopted, with NAFLD and NASH replaced by MASLD and MASH. The first treatment for MASH with demonstrated histological improvement, including fibrosis reduction, has reached the clinic. Single-cell technologies have transformed our understanding of fibrogenic cell populations and the gut–liver axis. Many questions from Volume I remain open, and many new ones have emerged.Despite substantial progress, inflammation and fibrosis remain the principal drivers of the progression of chronic gastrointestinal and liver diseases and continue to limit therapeutic success. Although advances in single-cell omics, spatial biology, organoid models, and systems immunology have uncovered previously unrecognized cellular heterogeneity and intercellular communication networks, translating these discoveries into effective diagnostic and therapeutic strategies remains a major challenge. Furthermore, the adoption of the MASLD/MASH nomenclature has highlighted the need to reassess disease mechanisms across diverse etiologies while identifying shared inflammatory and fibrotic pathways that may be therapeutically targeted. This Research Topic aims to provide an updated platform for multidisciplinary studies that advance our understanding of inflammatory and fibrogenic mechanisms throughout the gastrointestinal tract and liver. We welcome original research, reviews, and translational studies addressing immune regulation, stromal cell biology, extracellular matrix remodeling, gut–organ communication, metabolic and microbial influences, biomarker discovery, and emerging therapeutic approaches. By integrating mechanistic insights with clinical perspectives, this collection seeks to identify common pathogenic principles, highlight innovative technologies, and accelerate the development of precision medicine strategies for inflammatory and fibrotic diseases.Topics of interest include:• Fibrogenesis and Cellular Mechanisms: Hepatic stellate cell and fibroblast heterogeneity, macrophage polarisation, the GREM1–VEGFR2 axis in intestinal fibrosis, cellular senescence, and cell death pathways, including pyroptosis and ferroptosis.• Metabolic Drivers of Disease: The role of metabolic dysfunction in MASLD progression, bile acid dysregulation, NLRP3 inflammasome activation, lipid metabolism, and individual susceptibility to fibrotic disease.• Gut–Liver Axis: Microbial metabolites, intestinal barrier dysfunction, EV signalling between the gut epithelium and hepatocytes, microbiome restoration strategies, and neuro-immune interactions in disease progression.• Immune Regulation: Noncanonical NF-κB signalling in IBD, Th17/Treg balance, cytokine networks, including IL-6 as a predictor of biologic response, and mechanisms of anti-TNF failure.• Non-invasive Diagnostics: Multi-omics biomarkers, CEUS and elastography for fibrosis staging, liquid biopsy approaches, and AI-assisted histological assessment for monitoring disease activity and treatment response.• Emerging Therapies: THR-β agonists, GLP-1 receptor agonists, SGLT2 inhibitors, direct-acting antifibrotic agents in development, JAK inhibitors and S1P receptor modulators in IBD, and EV-based drug delivery.• Surgery and Endoscopy: Bowel-sparing and liver-preserving strategies in the context of expanding pharmacological options, changing surgical rates, and the inflammatory and fibrotic consequences of surgical intervention itself. Topic editors: Ralf Weiskirchen, Haibo Dong Source: https://www.frontiersin.org/research-topics/84616/inflammation-and-fibrosis-in-the-gastrointestinal-tract-and-liver-volume-ii