City of Detroit, Estados Unidos
Although the gastric mucosa of healthy adu lt a nima ls possesses the inhe re nt capacity to promptl y repa ir (ofte n within 24 h) after a mino r to moderate injury, agi ng 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 slowe r process is replacement of lost cells by ce ll division. Intrace llul a r eve nts that regul ate these processes are poorl y understood, nor do we know how they may be affected by aging. However, evidence is accumul ating which suggests that a number of gastro int esti na l hormones/grow th factors, most notabl y EGF and TGF-a may playa critical rol e in regul ati ng gastri c mucosal reparative processes. Since EGF and TGF-a exe rt the ir ph ysio logical actions by activating the intrinsic tyrosine kinase (Tyr-k) activity of their common receptor, the EGF-R, studi es have been performed to assess th e ro le of EG F-R Ty r-k in regul ating mucosal reparative processes during aging.
Rece nt data s uggest th a t the age -re la ted dec lin e in mucosal repair after acute injury could in part be due to dec rease d ac tivation of EGF-R Tyr-k. In ad dition , polyamines and prostaglandins are also thought to be inv o lved in gastric mucosa l repara ti ve processes.
A ltho ug h the involveme nt of po lyamin es in gastri c mucosal reparative processes during aging has not yet been studi ed, decreased mucosal prostaglandin levels in the aged are tho ught 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.
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