There was no significant change in miR-133, miR-30, or miR-101 family members after LPS. There was a transient increase in miR-21 on day 3 by miR expression profiling, which was not significant when measured by QRT-PCR. The most consistent change in fibrosis-related miRs was a significant decrease in miR-29c on miR expression profiling, which was confirmed by QRT-PCR, and persisted from 3 to 7 days after LPS. There was no significant change in miR-29a or miR-29b. The Taurocholic Acid sodium hydrate miR-29 family is the fourth most abundant miR in the heart, with preferential expression in fibroblasts. The miR-29 family includes 3 members expressed from a bicistronic cluster with miR-29a coexpressed with miR-29b-1, and miR-29b2 coexpressed with miR-29c. All three miR-29 family members are downregulated with myocardial ischemia-reperfusion in mice and humans, particularly in the border zone. A number of fibrosis-related genes are targeted by miR-29, including collagens, fibrillins, and elastin to induce cardiac fibrosis. In vivo inhibition of miR-29 with an Tamsulosin antagomir, an oligonucleotide complementary to miR-29b, activates collagen expression. Circulating miRs may be elevated in cardiac diseases and serve as biomarkers. In patients with hypertrophic cardiomyopathy, several miRs, including miR-29a, are elevated and correlate with ventricular remodeling and the degree of cardiac hypertrophy Only miR-29a correlated with the extent of cardiac fibrosis, as measured by cardiac magnetic resonance. miR-29 plays a role in fibrosis also in the liver. LPS from the gut exacerbates hepatic fibrosis after chemical injury. Hepatic stellate cells, the major cell in hepatic fibrogenesis, are rapidly activated by LPS to decrease miR-29a, miR-29b, and miR29c. The gut is the source of subclinical LPS in metabolic endotoxemia. It is unknown if LPS from the gut plays a similar role to decrease cardiac miR-29c in cardiac fibrosis. Subclinical LPS induced cardiac fibrosis without preceding myocardial injury, in contrast to exacerbation of hepatic fibrosis induced by chemical injuries. The miR-29 family directly regulates at least 16 extracellular matrix genes.