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Organ fibrosis is a complex and chronic disorder that results from a variety of acute injuries and contributes to thirty percent of naturally occurring deaths worldwide. The main feature of organ fibrosis is the excessive accumulation and deposit of extracellular matrix, thereby leading to organ dysfunction, loss of elasticity, and development of a rigid organ. Accumulating evidence shows that epigenetic remodeling, including aberrant DNA methylation and noncoding RNA expression as well as histone post-translational modifications, play important roles in the pathogenesis of fibrosis through the regulation of fibroblast activation, differentiation, and apoptosis, as well as collagen synthesis and profibrotic gene transcription. In this review, we discuss the basic regulation of DNA methylation, noncoding RNA expression, and histone post-translational modification, and their participation in the pathogenesis and development of organ fibrosis. This review also provides the latest insights into the novel biomarkers and therapeutic targets for fibrosis through modulation of epigenetic remodeling., (Copyright © 2014 by The American Society for Pharmacology and Experimental Therapeutics.)

'Transient receptor potential (TRP) channels are cellular sensors for a wide spectrum of physical and chemical stimuli. Activation of TRP channels changes the membrane potential, translocates important signaling ions crossing the cell membrane, alters enzymatic activity, and initiates endocytosis/exocytosis (Zheng, 2013).' Fibrosis is the leading cause of organ dysfunction in diseases, which is characterized by an imbalance in the turnover of extracellular matrix components. Accumulating evidence has demonstrated that TRPM7, a member of TRP channels superfamily, participates in the development and pathogenesis of fibrotic diseases, such as hepatic, pulmonary and cardiac fibrosis. In this review, we discuss the comprehensive role of TRPM7 in modulating profibrotic response and its potential as therapeutic target for fibrotic diseases. J. Cell. Physiol. 230: 1163-1169, 2015. © 2014 Wiley Periodicals, Inc., A Wiley Company [ABSTRACT FROM AUTHOR]