ReviewFrontiers in cell and developmental biology2026
Early life stress and the pathogenesis of visceral hypersensitivity: mechanisms and implications for disorders of gut-brain interaction.
Review in Frontiers in cell and developmental biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Early life stress (ELS) is a major risk factor for disorders of gut-brain interaction (DGBIs), particularly irritable bowel syndrome (IBS), through the induction of persistent visceral hypersensitivity. This review synthesizes evidence from epidemiological studies, clinical observations, and preclinical models to establish ELS-induced visceral hypersensitivity as a core pathophysiological axis. I delineate the multi-level mechanisms underlying this phenomenon, encompassing: (1) central neuroendocrine dysregulation (hypothalamic-pituitary-adrenal axis, corticotropin-releasing factor signaling) with epigenetic modifications (histone acetylation, non-coding RNAs) in limbic circuits; (2) spinal sensitization via brain-derived neurotrophic factor upregulation, glutamate transporter dysfunction, and potassium channel downregulation; (3) peripheral alterations including enterochromaffin cell hyperplasia, mast cell activation, enteric glial phenotypic switching, barrier disruption, and microbiota dysbiosis. I highlight critical modifiers including sexual dimorphism (estrogen-dependent mechanisms) and resilience factors (benevolent childhood experiences, environmental enrichment). Finally, I present a translational roadmap integrating pharmacological, nutritional, and behavioral interventions targeting ELS-programmed dysfunction along the brain-gut axis, emphasizing opportunities for prevention and precision medicine.
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