These early events are followed by extracellular matrix destruction and remodelling, vascular smooth muscle cell depletion and dysfunction. Experiments had demonstrated that Hcy stimulates chemokine and cytokine secretion from cultured human monocytes and has been implicated in suppressing regulatory T-cell function. A recent interesting study by Liu Z et al., within an angiotensin II induced AAA mouse model suggests that hyper-Hcy exaggerates adventitial inflammation, promoting AAA. Hcy induces the synthesis of serine elastase in arterial smooth muscle cells, causing elastolysis by degradation of the extracellular matrix and release of reactive oxygen species, which are implicated in AAA pathogenesis. Whether Hcy plays a role in aneurysm formation and/or in aneurysm expansion or Hcy is simply a marker of the condition need to be investigated. Plasma Hcy levels are also influenced by several factors such as genetic factors, plasma folate and vitamin B12 concentrations. Selhub and colleagues have suggested that inadequate plasma concentrations of one or more B vitamins are contributing factors in approximately two thirds of all cases of hyperhomocysteinaemia and that vitamin supplementation can normalise high homocysteine concentrations. As lack of well-designed RCTs, we were unable to perform a meta-analysis of the clinical effects of Hcy-lowering therapy among the limited studies because of the in consistent outcomes. Hcy-lowering therapy by folic acid, vitamins B6 and B12 supplement will help to reduce rates of AAA or not, the answer maybe urgent in the development of interventions to prevent AAA. More well-design RCTs are needed to test the effects of Hcy-lowering therapy on the AAA incident. Although we only included the case-control studies in the analysis, there are still several potential limitations. First, because of the cross-sectional design, the studies are unable to determine if the altered parameters are causally related to the presence of AAA. Second, we only included the study in English and Chinese, and some relevant studies might be not included in the review. There was a low risk of publication bias in studies of Hcy concentrations in relation to all AAA, as suggested by asymmetrical funnel plot on visual inspection and Egger’s linear regression test. Third, there was significant heterogeneity among the included studies. Another potential source of heterogeneity was the lack of uniform definition of subjects. Forth, a major limitation was the possibility of uncontrolled confounding, and the individual studies did not adjust for potential risk factors in a consistent way. A wide spectrum of diseases was associated with elevated plasma Hcy concentrations, such as cardiovascular 9-methoxycamptothecine disease, stroke and cognitive impairment. These diseases were also associated with AAA; some residual confounding factors still affected the Salvianolic-acid-B results. None of the analyzed studies seems to have adjusted Hcy levels for its most important covariate, glomerular filtration rate, and this is a major problem for the outcome. The lack of adjustment for these confounding factors might have resulted in a slight over estimation of the OR. Finally, the studies of Wong YYE and the Brunelli T contained only men, and that may make the findings have only limited relevance to AAA in women. Chronic, low-grade inflammation in adipose tissue induced by obesity is characterized by an aberrant release of hormones, cytokines and chemokines. These factors affect insulin sensitivity not only in an auto-/paracrine fashion in adipose tissue but also in an endocrine manner in liver and skeletal muscle.