title: Regulatory Mechanisms of the Molecular Pathways in Fibrosis Induced by MicroRNAs.
abstract: 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.
  
  
  METHODS
  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".
  
  
  METHODS
  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.
authors.affiliation: Department of Cardiology, Huairou Hospital of Traditional Chinese Medicine, Beijing 101400, China.
authors.forename: Cui
authors.initials: C
authors.lastname: Yang
authors.affiliation: Department of Cardiology, Beijing Hospital of Integrated Traditional Chinese and Western Medicine, Beijing 100039, China.
authors.forename: Si-Dao
authors.initials: SD
authors.lastname: Zheng
authors.affiliation: Department of Cardiology, Beijing Haidian Hospital, Haidian Section of Peking University Third Hospital, Beijing 100191, China.
authors.forename: Hong-Jin
authors.initials: HJ
authors.lastname: Wu
authors.affiliation: Department of Cardiology, Huairou Hospital of Traditional Chinese Medicine, Beijing 101400, China.
authors.forename: Shao-Jun
authors.initials: SJ
authors.lastname: Chen
mesh_terms: D000818:Animals; D048049:Extracellular Signal-Regulated MAP Kinases / Q000235:genetics / Q000378:metabolism; D005355:Fibrosis / Q000235:genetics* / Q000378:metabolism*; D006801:Humans; D035683:MicroRNAs / Q000235:genetics*; D020928:Mitogen-Activated Protein Kinases / Q000235:genetics / Q000378:metabolism; D016212:Transforming Growth Factor beta / Q000235:genetics / Q000378:metabolism
chemical_list: D035683:MicroRNAs; D016212:Transforming Growth Factor beta; D048049:Extracellular Signal-Regulated MAP Kinases; D020928:Mitogen-Activated Protein Kinases