Inhibition of the miR-1914-5p increases the oxidative metabolism in cellular model of steatosis by modulating the Sirt1-PGC-1α pathway and systemic cellular activity.

Metabolic associated fatty liver disease (MAFLD) is considered an indicator of metabolic syndrome, which affects millions of people around the world and no effective treatment is currently available. MAFLD involves a wide spectrum of liver damage, that initiates from steatosis (fatty live) and may progress to more complex pathophysiology. Then, details in lipid metabolism controlling should be explored aiming to control the fatty liver.

Non-alcoholic fatty liver disease: molecular and cellular interplays of the lipid metabolism in a steatotic liver.

Introduction: Non-alcoholic fatty liver disease (NAFLD) affects ~25% of world population and cases have increased in recent decades. These anomalies have several etiologies; however, obesity and metabolic dysfunctions are the most relevant causes. Despite being considered a public health problem, no effective therapeutic approach to treat NAFLD is available.

Variation in community structure of gall-inducing insects associated with a tropical plant supports the hypothesis of competition in stressful habitats.

Environmental factors act as drivers of species coexistence or competition. Mesic environments favor the action of parasites and predators on gall communities, while the factors that determine the structure of gall communities in xeric environments remain unknown. We evaluated the structure of gall communities along an environmental gradient defined by intrinsic plant characteristics, soil fertility, and aridity, and investigated the role of competition as a structuring force of gall communities in xeric environments.

The modulatory effect of triclosan on the reversion of the activated phenotype of LX-2 hepatic stellate cells.

Hepatic diseases leading to fibrosis affect millions of individuals worldwide and are a major public health challenge. Although, there have been many advances in understanding hepatic fibrogenesis, an effective therapy remains elusive. Studies focus primarily on activation of the hepatic stellate cells (HSCs), the principal fibrogenic cells in the liver; however, fewer numbers of studies have examined molecular mechanisms that deactivate HSC, controlling the profibrogenic phenotype.

MicroRNA-1254 contributes to the controlling of pro-fibrogenic environment in LX-2 cells by modulating SMAD3 and wound repair: new insights in hepatic fibrosis.

Hepatic fibrosis and its end-stage cirrhosis have increased worldwide, and, despite all the efforts, no successful therapy is available. More recently, the heptapeptide angiotensin-(1-7) [ang-(1-7)] was reported to be able to modulate liver fibrosis and even steatosis; however, the molecular bases of these effects are not clear. In this study, we investigated the overexpression of the microRNA-1254 in the human hepatic stellate cell line LX-2, based on the effect of the heptapeptide in such cells, previously, demonstrated by our research group.

Altered global microRNA expression in hepatic stellate cells LX-2 by angiotensin-(1-7) and miRNA-1914-5p identification as regulator of pro-fibrogenic elements and lipid metabolism.

The development of new therapeutic strategies to control or reverse hepatic fibrosis requires thorough knowledge about its molecular and cellular basis. It is known that the heptapeptide angiotensin-(1-7) [ang-(1-7)] can reduce hepatic fibrosis and steatosis in vivo; therefore, it is important to uncover the mechanisms regulating its activity and cellular model of investigation. Ang-(1-7) is a peptide of the renin-angiotensin system (RAS), and here we investigated its modulatory effect on the expression pattern of microRNAs (miRNAs) in hepatic stellate cells (HSCs) LX-2, which transdifferentiate into fibrogenic and proliferative cells.

Molecular interplays in hepatic stellate cells: apoptosis, senescence, and phenotype reversion as cellular connections that modulate liver fibrosis.

Liver fibrosis is a pathophysiological process correlated with intense repair and cicatrization mechanisms in injured liver, and over the past few years, the characterization of the fine-tuning of molecular interconnections that support the development of liver fibrosis has been investigated. In this cellular process, the hepatic stellate cells (HSCs) support the organ fibrogenesis. The HSCs are found in two distinct morpho-physiological states: quiescent and activated.