Retinopathy is a severely disabling complication of diabetes mellitus
whose underlying mechanisms are still obscure. The key question is why
retinal microvessels are so reactive to the diabetic environment, whe
reas other microvessels show no evidence of alteration. The answer cou
ld lie in the particular structure and location of retinal microvessel
s since they are composed of, and surrounded by, various types of cell
s, thereby favouring cell-cell interactions which occur between cells
of the capillary wall itself but also with circulating blood cells and
retinal neural cells. In the retinal capillary wall, pericytes are in
close relation with underlying endothelial cells, and both cell types
have close contacts with the capillary basement membrane. Adhesion mo
lecules and cell surface glycoconjugates appear to be the main mediato
rs of interactions between circulating blood cells and capillary endot
helial cells, whereas growth factors seem to play a major role in inte
ractions between glial and capillary wall cells in the retina. Biochem
ical dysfunctions observed in diabetes, such as glycation of proteins
and enhanced oxidative stress, could modify these cell-cell and cell-m
atrix interactions, thereby disturbing the complex cellular organizati
on in which retinal microvessels are embedded. The aim of this review
was to provide an overall, nonexhaustive description of some types of
cellular interactions that may underlie the pathogenic mechanisms invo
lved in flow and growth changes leading to diabetic retinopathy.