And this pathological process finally leads to a disorder of lens short-circuit current that plays a protective role against cataract formation. Results from Ornek et al. showed that hypertensive patients would have a significantly higher level of nitrite in their cataractous lenses; the resulting nitric oxide plays an important role in the pathogenesis of human cataract. What’s more, Johnson et al. reported a novel gene mutation related to both cataract and hypertension, which may be helpful in finding the potential fundamentals of genetics. Heterogeneity was detected by means of Cochran’s Q statistic and I2 score among the BAY-60-7550 studies included in this meta-analysis., which might be caused by different adjustments for confounders, the various ages of the study populations, different sample sizes, and various cataract criteria. We performed a metaregression analysis to assess the effect of sample size, study design, study conducted race, publication year and cataract criteria on the heterogeneity, but none was identified as the main source of heterogeneity. The existence of heterogeneity indicates the need for unified methodologies in future studies. Our meta-analysis has several strengths. Not only cross-sectional or casecontrol studies but also cohort studies were included in this analysis; the latter tends to be insusceptible to selection bias. Each study was adjusted for age, which is the most reliable independent risk factor for cataract. Most studies included in our meta-analysis were based on the general population for more generalizable results. In addition, we performed a subgroup analysis to rule out the influences of pathoglycemia, obesity and dyslipidemia, which are thought to be the common risk factors for both hypertension and cataract. Potential limitations of our meta-analysis, which may affect the interpretation of results, should be mentioned. Firstly, the assessment of cataract and adjusted factors varied among the studies, contributing to an increase of heterogeneity.Simultaneously Nox2-dependent ROS generation by activated LOX-1 stimulates intracellular signaling, namely, p38 MAPK and NF-kB, which upregulates gene expression of adhesion molecules and cytokines. We also found that less phosphorylation of p38 MAPKs and NF-kB, major downstream signaling factors of LOX-1, was observed in ischemic limb of LOX-1 KO mice than in that of WT mice. In this experiment, inhibition of NF-kB activation by LOX-1 deletion caused less VCAM-1 expression in endothelial cells, which reduces macrophage infiltration into the ischemic tissue. Importantly, LOX-1 also plays a role as an adhesion molecule and then Infiltration of macrophages is supposed to be more significant in WT mice than in LOX-1 KO mice in the ischemic hindlimb.