Gastric mucosal injury and repair, effect of aging

Abstract

Although the gastric mucosa of healthy adult animals possesses the inherent capacity to promptly repair (often within 24 h) after a minor to moderate injury, aging appears to diminish its reparative capacity. At least two different repair mechanisms are thought to participate in full repair of the damaged gastric mucosa: the initial rapid process of mucosal restitution begins by migration of viable epithelial cells from gastric pits and glands; the subsequent slower process is replacement of lost cells by cell division. Intracellular events that regulate these processes are poorly understood, nor do we know how they may be affected by aging. However, evidence is accumulating which suggests that a number of gastrointestinal hormones/growth factors, most notably EGF and TGF-a may play a critica1 role in regulating gastric mucosal reparative processes. Since EGF and TGF-a exert their physiological actions by activating the intrinsic tyrosine kinase (Tyr-k) activity of their common receptor, the EGF-R, studies have been performed to assess the role of EGF-R Tyr-k in regulating mucosal reparative processes during aging. Recent data suggest that the age-related decline in mucosal repair after acute injury could in part be due to decreased activation of EGF-R Tyr-k. In addition, polyamines and prostaglandins are also thought to be involved in gastric mucosal reparative processes. Although the involvement of polyamines in gastric mucosal reparative processes during aging has not yet been studied, decreased mucosal prostaglandin levels in the aged are thought to be a causative factor for the increased susceptibility of the mucosa to injury. These and other relevant matters are discussed in the current review.