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The identification of non-coding RNA species, previously thought of as 'junk' DNA, adds a new dimension of complexity to the regulation of DNA, RNA and protein. Micro RNAs are short non-coding RNA species that control gene expression, are dysregulated in settings of cardiac and skeletal muscle disease and have emerged as promising therapeutic targets. Micro RNAs specifically enriched in cardiac and skeletal muscle are called myomiRs and play an important role in cardiac pathology and skeletal muscle biology. Moreover, micro RNA profiles are altered in response to exercise and disease; thus, their potential as therapeutic drug targets is being widely explored. In the cardiovascular field, therapeutic inhibition of micro RNAs has been shown to be effective in improving cardiac outcome in preclinical cardiac disease models. Micro RNAs that promote skeletal muscle regeneration are attractive therapeutic targets in muscle wasting conditions where regenerative capacity is compromised. [ABSTRACT FROM AUTHOR]

Although micro RNAs (mi RNAs) have been recognized as one of the important epigenetic mechanisms that regulate gene expression in response to changes in the environment, the links between environmental cues and changes in mi RNAs remain largely unknown. Localized to the cell membrane and recognized as an anion channel, the cystic fibrosis transmembrane conductance regulator ( CFTR) has recently been shown to mediate important signalling pathways leading to activation of mi RNAs. This brief review summarizes the related findings and discusses the emerging role of CFTR as an epigenetic regulator, possibly involved in a wide spectrum of physiological and pathological processes. [ABSTRACT FROM AUTHOR]

Diabetic nephropathy ( DN) is a major diabetic complication that is mediated by transforming growth factor ( TGF)-β1 via Smad-dependent and -independent signalling pathways., Under diabetic conditions, many profibrotic factors, such as advanced glycation end-products and angiotensin II, can also activate the Smad signalling pathway via the extracellular signal-regulated kinase/p38 mitogen-activated protein kinase- Smad signalling cross-talk pathway. Thus, Smads act as signal integrators and interact with other signalling pathways to mediate DN., In the context of renal fibrosis, Smad3 is pathogenic, but Smad2 is protective. Deletion of Smad3 inhibits, whereas disruption of Smad2 upregulates, connective tissue growth factor and vascular endothelial growth factor expression and promotes both epithelial-myofibroblast and endothelial-myofibroblast transition., Smad7 plays a protective role in DN because deletion of Smad7 enhances, whereas overexpression of Smad7 inhibits, Smad3-mediated renal fibrosis and nuclear factor-κ B-driven renal inflammation., Transforming growth factor-β1 activates Smad3 to regulate micro RNAs that mediate renal fibrosis. Of these, mi R-21 and mi R-192 are upregulated, whereas the mi R-29 and mi R-200 families are downregulated., Targeting downstream TGF-β/ Smad signalling by overexpressing Smad7- or Smad3-dependent micro RNA related to fibrosis may represent a novel and effective strategy for the treatment of DN. [ABSTRACT FROM AUTHOR]