Cellular Senescence and Ageing of the Gastrointestinal Tract: Mechanisms, Functional Alterations, and Nutritional Implications—Literature Review

Ageing of the gastrointestinal tract—also termed gastrosenescence—results from the interplay between the accumulation of senescent cells and the structural, functional, and microbiological changes characteristic of old age. Cellular senescence, defined by permanent cell-cycle arrest and an associated secretory phenotype (SASP), plays a dual role: it facilitates the clearance of damaged cells and acute tissue repair, yet, when persistent, it promotes chronic inflammation, fibrosis, and a protumoural microenvironment. The intestinal microbiota and its genotoxic metabolites modulate senescence and SASP, thereby influencing colorectal and hepatic carcinogenesis. Along the digestive tract, age-related changes include loss of taste and dentition, hypochlorhydria, variable gastric emptying, malabsorption—particularly of lactose—and slowed colonic transit, all of which contribute to the anorexia of ageing, protein-energy malnutrition, and sarcopenia. Histologically, an imbalance between proliferation and apoptosis and hormonal alterations predispose to neoplastic development. Optimal management requires a multidisciplinary approach encompassing detection of senescence biomarkers, senolytic and senostatic therapies, microbiota modulators, dietary texture adaptation, specialised supplementation, and correction of micronutrient deficiencies. This integrated strategy may improve quality of life, reduce complications, and optimise prognosis in geriatric patients with gastrointestinal disorders.