MicroRNA‐21 and Dicer are dispensable for hepatic stellate cell activation and the development of liver fibrosis

Abstract

Genetic and pharmacologic manipulation of miR-21 does not inhibit the development of liver fibrosis and liver cancer. Moreover, suppression of microRNA synthesis does not significantly affect HSC phenotype and activation. (Hepatology 2018;67:2414-2429).

Is miR‐21 a potent target for liver fibrosis?

“…In contrast to these studies (Table ), in the current issue of H epatology , Caviglia et al report that miR‐21 is not crucial for the activation of hepatic stellate cells (HSCs) or the development of liver fibrosis. To reach this conclusion, the investigators performed rigorous examinations with genetic and pharmacologic manipulation of miR‐21 in multiple models of liver fibrosis.…”

Long noncoding RNA HOTTIP mediates SRF expression through sponging miR‐150 in hepatic stellate cells

“…Hepatic stellate cell (HSC) activation is regarded as the important event in the progression of liver fibrosis . Recently, it has been reported that many noncoding RNAs have been linked to HSC activation . However, the function and underlying mechanism of noncoding RNAs in liver fibrosis is far from being fully elucidated.…”

Inflammasomes and their roles in the pathogenesis of viral hepatitis and their related complications: An updated systematic review

“…Angiotensin II and HSCs are the main responsible parameters involved in the fibrosis of the liver [66,67]. Moreover, the roles played by microRNA-21 in the induction of liver fibrosis have been documented previously [68,69]. For instance, it has been reported that transforming growth factor beta (TGF-β) is an important molecule, which participates in the induction of inflammation and also fibrosis in the liver via interaction with receptor-regulated SMAD (mothers against decapentaplegic drosophila homolog) proteins (R-SMADs) [4,70].…”

“…It has been documented that mitophagy is a biological process to remove the dysfunctional mitochondria, which is a main cause of cancers [84]. FUN14 domain containing 1 (FUNDC1), a well-characterized mitophagy receptor, mediates mitophagy and consequently suppresses HCC induction through inhibition of inflammasome activation, including caspase-1 and IL-1β [68]. Additionally, it has been demonstrated that increased background non-tumorous hepatocyte levels of NLRP3, NLRC4, and caspase-1 have significant correlations with poor HCC prognosis [85].…”