Esophageal Diseases: Molecular Basis and Therapeutic Approaches

Dear Colleagues,

The esophagus hosts inflammatory and neoplastic disorders, including gastroesophageal reflux diseases, eosinophilic esophagitis, Barrett’s esophagus, esophageal adenocarcinoma, and squamous cell carcinoma. When affecting aging individuals, esophageal cancers are the deadliest of all human cancers. When affecting both children and adults, chronic diseases like eosinophilic esophagitis have a life-long impact on growth and quality of life. These diseases are often associated with racial disparity. Food allergens, alcohol, and tobacco smoke constituents are among the environmental factors that may affect esophageal mucosal integrity in concert with genetic and epigenetic factors. The development and progression of esophageal diseases involve the perturbation of homeostatic epithelial renewal, squamous differentiation, epithelial barrier functions, and alterations in characteristics of epithelial cells (keratinocytes), as well as the subepithelial stromal compartment (connective tissue) comprising fibroblasts, muscle cells, endothelial cells, immune cells, and the extracellular matrix. Many esophageal disease conditions feature robust tissue remodeling, as exemplified by intestinal metaplasia in the Barret’s esophagus, basal cell hyperplasia and fibrosis in eosinophilic esophagitis, and invasive tumor growth of esophageal cancers. These processes involve changes in broad biological processes such as cell proliferation, differentiation, de-differentiation (epithelial–mesenchymal transition), apoptosis, autophagy, and metabolism, along with associated molecular changes (e.g., DNA damage, protein phosphorylation, gene mutations, functional single-nucleotide polymorphism) and damages to or dysfunction of organelles (e.g., mitochondria). Additionally, these processes are subjected to regulation by specific growth factors and inflammatory cytokines, signaling pathways, downstream second messengers (e.g., reactive oxygen species), and transcriptional factors. Some of these are targetable for therapeutic interventions. Experimental studies of these esophageal diseases have utilized animal models and cell culture models, including genetically engineered mouse models and a three-dimensional organoid system, the latter serving as a physiologically relevant experimental platform that recapitulates original tissues in morphology and gene expression functions and therapy response, and is translatable to personalized medicine. This Special Issue will cover all topics related to the molecular pathogenesis of esophageal diseases, experimental platforms, and novel therapeutic approaches explored in preclinical and clinical settings. This Special Issue will consider f both review articles and original research articles for publication.

Dr. Hiroshi Nakagawa
Dr. Amanda B. Muir
Guest Editors

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