The results of this current meta-analysis indicated that the increased level of ICAM-1 generally exists in the patients with DR and it may associated with the severity of DR.
The downstream exacerbating factors including vascular endothelial growth factor (VEGF), intercellular adhesion molecule 1 (ICAM-1) and matrix metalloproteinase 2 (MMP2), which are implicated in the pathogenesis of DR and closely related to oxidative stress were also analyzed.
In conclusion, treatment with Niaspan significantly improved clinical and histopathological outcomes; decreased the expression levels of TNF‑α, NF‑κB, iNOS and ICAM‑1; and decreased apoptosis and BRB breakdown, as compared with in the retinas of DR rats.
Inhibition or knock down of endothelial 12/15-LO in HRECs blocked HG-induced expression of ICAM-1, a well-known identified important molecule for leukocyte adhesion in DR.
The data indicated that TUDCA could ameliorate DR by decreasing NO content and down-regulating the protein expression of ICAM-1, NOS, NF-κB p65 and VEGF.
Our results revealed that SNP rs5498 in ICAM-1 gene and IVS5-13insC variant in HMGA1 gene were not associated with the susceptibility of DR in the Chinese T2DM cohort.
A number of studies evaluated the association of intracellular adhesion molecule-1 (ICAM-1) K469E (rs5498, A/G) gene polymorphism with diabetic microvascular complications (DMI) including diabetic nephropathy (DN) and diabetic retinopathy (DR) in different populations.
A significantly higher frequency of the EE genotype of the K469E polymorphism of the ICAM-1 was found in the patients with PDR compared with those without diabetic retinopathy (OR = 2.0, 95% confidence interval [CI] = 1.1-3.5; P = 0.013), whereas the G241A polymorphism of the ICAM-1 gene failed to yield an association with PDR.
A significantly higher frequency of the EE genotype of the K469E polymorphism of the ICAM-1 was found in the patients with PDR compared with those without diabetic retinopathy (OR = 2.0, 95% confidence interval [CI] = 1.1-3.5; P = 0.013), whereas the G241A polymorphism of the ICAM-1 gene failed to yield an association with PDR.
The frequency of ICAM-1 469KK genotype and K allele were significantly higher in the patients with diabetic retinopathy than in those without retinopathy (genotype 42% vs. 20%, chi2 = 6.70, P = 0.035; allele 66% vs. 50%, chi2 = 6.49, P = 0.011).
The frequency of ICAM-1 469KK genotype and K allele were significantly higher in the patients with diabetic retinopathy than in those without retinopathy (genotype 42% vs. 20%, chi2 = 6.70, P = 0.035; allele 66% vs. 50%, chi2 = 6.49, P = 0.011).
These data identify the causal role of leukocytes in the pathogenesis of diabetic retinopathy and establish the potential utility of ICAM-1 inhibition as a therapeutic strategy for the prevention of diabetic retinopathy.
Binary logistic regression displays that the association of the ACE and AGT gene polymorphisms in DR patients is not significant after adjusting for confounding covariates in all the comparisons.