Since decreased miR-29c and increased NOX2 precede activation of other fibrotic factors and are associated with cardiac fibrosis in other Lenalidomide hemihydrate conditions, this suggests a unique role of miR-29c and NOX2 in LPS-induced cardiac fibrosis. There was no evidence of cardiac hypertrophy, with no significant difference in LV weight normalized to body weight between any of the groups. Data for the combined right and left ventricle were similar, with no evidence of hypertrophy at any time period. This is similar to prior results showing no evidence of cardiac hypertrophy after 12�C15 weeks of LPS. Figure 1 shows a representative example of photomicrographs of picrosirius red-stained sections from the left ventricle at the midventricular level after i.p. saline, 1, 2, or 4 weeks of LPS. The fibrosis was mostly interstitial and occasionally perivascular with no obvious transmural differences, although this was not systematically examined. Figure 2 shows Pamidronate disodium pentahydrate collagen fraction area in the left ventricle, measured by pircrosirius staining increased after 2 and 4 weeks of LPS, compared with control or 1 week after LPS. This was similar to the increase in LV collagen fraction area observed after 3 months of weekly LPS. To assess which profibrotic factors are activated early after LPS, measurements were made in two groups of mice three days after injection of LPS or saline. The major findings of this study are that exposure to subclinical LPS activates mediators in the heart within days, with activation of pro-fibrotic factors after one week leading to cardiac fibrosis after two weeks. The earliest changes are decreased cardiac expression of miR-29c with increased IL-6, NOX2, and TIMP1 three days after LPS. After one week, there was increased cardiac expression of collagen Ia1, collagen IIIa1, TIMP2, MMP2, and periostin, which persisted at two weeks. At two weeks there was an additional increase in MMP9 and cardiac fibrosis with increased collagen fraction area in the left ventricle. Cardiac structure is maintained by a dynamic balance of extracellular matrix proteins, including MMPs and TIMPs.