regulates inflammasome-mediated hypertensive cardiac inflammation and fibrosis .

Hypertension is a severe public health problem that induces cardiac injury with alterations of gene expressions. The current study sought to evaluate the mechanism of ( in NOD-like receptor family pyrin domain containing 3 () inflammasome-mediation of cardiac inflammation and hypertensive cardiac fibrosis. Firstly, hypertensive mouse models were established using angiotensin II (Ang II), followed by agomir treatment. Subsequently, mouse blood pressure and basic cardiac function indexes, histopathological changes, and cardiac fibrosis were all determined, in addition to detection of factors related to inflammation and fibrosis. Additionally, mice cardiac fibroblasts (CFs) were isolated and treated with Ang II. The binding relationship of and thioredoxin-interacting protein () was predicted and testified, while the interaction of and was detected by means of a co-immunoprecipitation assay. It was found that was poorly-expressed in Ang II-treated mice and further exerted cardioprotective effects against hypertensive heart diseases. Moreover, over-expression of resulted in inhibition of inflammatory infiltration and almost eliminated cardiac fibrosis, as evidenced by decreased Collagen (COL)-I, COL-III, a-smooth muscle actin, , tumor necrosis factor-α, and interleukin-6. Mechanically, inhibited expression to block the binding of and . On the other hand, up-regulation reversed the protective role of over-expression in CFs. Collectively, our findings indicated that over-expression inhibited expression to block the binding of and , thereby alleviating hypertensive cardiac inflammation and fibrosis.