Expression of matrix metalloproteinase-11 is increased under conditions of insulin resistance.

Aim: To investigate matrix metalloproteinase-11 () expression in adipose tissue dysfunction, using and models of insulin resistance.

Methods: Culture of mouse 3T3-L1 preadipocytes were induced to differentiation into mature 3T3-L1 adipocytes. Cellular insulin resistance was induced by treating differentiated cultured adipocytes with hypoxia and/or tumor necrosis factor (TNF)-α, and transcriptional changes were analyzed in each condition thereafter.

A polymorphism of HMGA1 protects against proliferative diabetic retinopathy by impairing HMGA1-induced VEGFA expression.

Diabetic retinopathy (DR) is a major complication of diabetes mellitus, and is the leading cause of blindness in working-age people. Usually, DR progresses from the asymptomatic non-proliferative DR that does not significantly alter vision, to proliferative DR (PDR), which can result in aberrant retinal neovessel formation and blindness. The High-Mobility-Group A1 (HMGA1) protein is a transcriptional master regulator of numerous genes, including metabolic and inflammatory genes, which, by modulating the expression of angiogenic factors, may induce retinal neovascularization, a hallmark of PDR.

HMGA1 is a novel candidate gene for myocardial infarction susceptibility.

Background: Acute Myocardial infarction (AMI), a leading cause of morbidity and mortality worldwide, is a dreadful acute complication of coronary atherosclerosis. Type 2 diabetes mellitus (T2DM) is associated with an increased risk of developing AMI. The architectural transcription factor high-mobility-group AT-hook 1 (HMGA1) has been involved in atherosclerosis, plaque formation, inflammation, and in the pathogenesis of insulin resistance and T2DM.