4 research outputs found
Gastric mucosal injury and repair, effect of aging
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