Down regulation of miR-29 activates several extracellular matrix proteins that play important roles in cardiac fibrosis. In the Saquinavir Mesylate kidney, downregulation of miR-29c is Methacycline HCl associated with renal interstitial fibrosis with increased collagen type II a1 and tropomyosin 1a, which are attenuated by activating hypoxia-inducible factor-a. Downregulation of miR29c in fibroblasts activates extracellular matrix genes resulting in fibrotic extracellular changes in idiopathic pulmonary fibrosis. Identifying the target sites and the role of miRs have generated considerable interest as manipulating miRs may be a novel therapeutic approach to treat cardiovascular diseases, including cardiac fibrosis. In the current study, low dose LPS markedly decreased miR29c in isolated cardiac fibroblasts. Since several fibrosis-related genes are directly activated by decreased miR-29, decreased miR-29c may play an important role in the LPS-induced cardiac fibrosis. Subclinical LPS may induce oxidative stress with reactive oxygen species. The NOX system is a major source of ROS in the heart. The NOX family contains 7 members, with NOX2 and NOX4 the predominant isoforms in the heart and expressed in cardiac myocytes, fibroblasts, and endothelial cells. LPS activates NOX4 to generate ROS in endothelial cells. Angiotensin II or aldosterone increase NOX2 activity to activate profibrotic genes with interstitial fibrosis. There are links between LPS responses and NOX. LPS increases NOX2- mediated ROS generation and MMP9 in macrophages, or NOX4-mediated increases in H2O2 and IL6 release in peripheral blood mononuclear cells. In acute lung injury, LPS causes endothelial dysfunction with increased vascular permeability by NOX2- and ROS-mediated pathways. In the current study, LPS increased cardiac NOX2, but not NOX4, after 3 days, which persisted after 1 and 2 weeks. In isolated cardiac fibroblasts, LPS dose-dependently increased NOX2 mRNA expression, which may be an important cellular target. It is possible that LPS activates NOX2 in other cells as well, which may play a potential role.