Objective：MicroRNAs （miRNAs or miRs） play critical roles in the fibrotic process in different organs.We summarized the latest research progress on the roles and mechanisms of miRNAs in the regulation of the molecul...Objective：MicroRNAs （miRNAs or miRs） play critical roles in the fibrotic process in different organs.We summarized the latest research progress on the roles and mechanisms of miRNAs in the regulation of the molecular signaling pathways involved in fibrosis.Data Sources：Papers published in English from January 2010 to August 2015 were selected from the PubMed and Web of Science databases using the search terms ＂microRNA＂,＂miR＂,＂transforming growth factor β＂,＂tgf β＂,＂mitogen-activated protein kinase＂,＂mapk＂,＂integrin＂,＂p38＂,＂c-Jun NH2-terminal kinase＂,＂jnk＂,＂extracellular signal-regulated kinase＂,＂erk＂,and ＂fibrosis＂.Study Selection：Articles were obtained and reviewed to analyze the regulatory effects of miRNAs on molecular signaling pathways involved in the fibrosis.Results：Recent evidence has shown that miRNAs are involved in regulating fibrosis by targeting different substrates in the molecular processes that drive fibrosis,such as immune cell sensitization,effector cell activation,and extracellular matrix remodeling.Moreover,several important molecular signaling pathways involve in fibrosis,such as the transforming growth factor-beta （TGF-β） pathway,mitogen-activated protein kinase （MAPK） pathways,and the integrin pathway are regulated by miRNAs.Third,regulation of the fibrotic pathways induced by miRNAs is found in many other tissues in addition to the heart,lung,liver,and kidney.Interestingly,the actions of many drugs on the human body are also induced by miRNAs.It is encouraging that the fibrotic process can be blocked or reversed by targeting specific miRNAs and their signaling pathways,thereby protecting the structures and functions of different organs.Conclusions：miRNAs not only regulate molecular signaling pathways in fibrosis but also serve as potential targets of novel therapeutic interventions for fibrosing diseases.展开更多
Objective To investigate the effect of blood-cooling and promoting drugs (BCPD) on the dynamic changes of collagens and the expressions of interleukin-6 (IL-6)and transforming growth factor beta (TGF-β) in lung tissu...Objective To investigate the effect of blood-cooling and promoting drugs (BCPD) on the dynamic changes of collagens and the expressions of interleukin-6 (IL-6)and transforming growth factor beta (TGF-β) in lung tissue of rats with radiation-induced lung injury (RILI) to explore the effects and action mechanism of BCPD in preventing and treating RILI. Methods One hundred and sixty Wistar female rats were randomly divided into the radiation group, the treatment group, the blank control group and the drug control group. The rats in the first two groups received right hemithoracic fractionated radiation, and those in the treatment group were given BCPD. Rats in the other two groups were not irradiated and BCPD was given to rats in the drug control group. The rats were sacrificed in batches (8 of each group in every batch) at the 3rd, 5th, 8th, 12th and 26th week of the experimental period, and their lung was taken for observing the dynamic changes and distribution of collagen and the expressions of IL-6 and TGF-β with HE staining, picrosirius red staining and immunohistochemical staining respectively. Results The fibroblast proliferated obviously from the 3rd week after the first radiation in the radiation group, and the type Ⅰ collagen and the proportion of type Ⅰ and Ⅲ collagen were significantly elevated along the time going and the radiation dose increasing, became significantly higher than those in the treatment group at all the time points (P<0.01). In the radiation group the expression of IL-6 and TGF-β reached their peaks at the 8th and 12th week, respectively, and the levels was significantly lower in the treatment than that in the radiation group at any detecting time points (P<0.01). Conclusion BCPD applied in the early stage of radiation can suppress the inflammatory and fibrogenic cytokine expressions, inhibit the synthesis of collagens and adjust the proportion of type Ⅰ and Ⅲ collagen, so as to relieve the early-stage inflammatory reaction and the anaphase lung fibrosis in RILI rats.展开更多
基金This study was supported by the grant from the Science Foundation for the Excellent Youth of Beijing （No. 2014000057592G296）.
文摘Objective：MicroRNAs （miRNAs or miRs） play critical roles in the fibrotic process in different organs.We summarized the latest research progress on the roles and mechanisms of miRNAs in the regulation of the molecular signaling pathways involved in fibrosis.Data Sources：Papers published in English from January 2010 to August 2015 were selected from the PubMed and Web of Science databases using the search terms ＂microRNA＂,＂miR＂,＂transforming growth factor β＂,＂tgf β＂,＂mitogen-activated protein kinase＂,＂mapk＂,＂integrin＂,＂p38＂,＂c-Jun NH2-terminal kinase＂,＂jnk＂,＂extracellular signal-regulated kinase＂,＂erk＂,and ＂fibrosis＂.Study Selection：Articles were obtained and reviewed to analyze the regulatory effects of miRNAs on molecular signaling pathways involved in the fibrosis.Results：Recent evidence has shown that miRNAs are involved in regulating fibrosis by targeting different substrates in the molecular processes that drive fibrosis,such as immune cell sensitization,effector cell activation,and extracellular matrix remodeling.Moreover,several important molecular signaling pathways involve in fibrosis,such as the transforming growth factor-beta （TGF-β） pathway,mitogen-activated protein kinase （MAPK） pathways,and the integrin pathway are regulated by miRNAs.Third,regulation of the fibrotic pathways induced by miRNAs is found in many other tissues in addition to the heart,lung,liver,and kidney.Interestingly,the actions of many drugs on the human body are also induced by miRNAs.It is encouraging that the fibrotic process can be blocked or reversed by targeting specific miRNAs and their signaling pathways,thereby protecting the structures and functions of different organs.Conclusions：miRNAs not only regulate molecular signaling pathways in fibrosis but also serve as potential targets of novel therapeutic interventions for fibrosing diseases.
文摘Objective To investigate the effect of blood-cooling and promoting drugs (BCPD) on the dynamic changes of collagens and the expressions of interleukin-6 (IL-6)and transforming growth factor beta (TGF-β) in lung tissue of rats with radiation-induced lung injury (RILI) to explore the effects and action mechanism of BCPD in preventing and treating RILI. Methods One hundred and sixty Wistar female rats were randomly divided into the radiation group, the treatment group, the blank control group and the drug control group. The rats in the first two groups received right hemithoracic fractionated radiation, and those in the treatment group were given BCPD. Rats in the other two groups were not irradiated and BCPD was given to rats in the drug control group. The rats were sacrificed in batches (8 of each group in every batch) at the 3rd, 5th, 8th, 12th and 26th week of the experimental period, and their lung was taken for observing the dynamic changes and distribution of collagen and the expressions of IL-6 and TGF-β with HE staining, picrosirius red staining and immunohistochemical staining respectively. Results The fibroblast proliferated obviously from the 3rd week after the first radiation in the radiation group, and the type Ⅰ collagen and the proportion of type Ⅰ and Ⅲ collagen were significantly elevated along the time going and the radiation dose increasing, became significantly higher than those in the treatment group at all the time points (P<0.01). In the radiation group the expression of IL-6 and TGF-β reached their peaks at the 8th and 12th week, respectively, and the levels was significantly lower in the treatment than that in the radiation group at any detecting time points (P<0.01). Conclusion BCPD applied in the early stage of radiation can suppress the inflammatory and fibrogenic cytokine expressions, inhibit the synthesis of collagens and adjust the proportion of type Ⅰ and Ⅲ collagen, so as to relieve the early-stage inflammatory reaction and the anaphase lung fibrosis in RILI rats.
