ABSTRACT
BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a deadly, chronic, progressive, irreversible interstitial lung disease characterized by the formation of scar tissue resulting in permanent lung damage. The average survival time following diagnosis is only 3-5 years, with a 5-year survival rate shorter than that of many cancers. Alveolar epithelial cell injury followed by irregular repair is the primary pathological process observed in patients with IPF. An evident characteristic of IPF is the development of fibroblastic foci representing active fibrotic areas. Most of the cells within these foci are believed to be myofibroblasts, which are thought to be the primary source of abnormal extracellular matrix production in IPF. The lung phenotype in IPF is characterized by significantly different processes from healthy lungs, including irregular apoptosis, oxidative stress, and epithelial-mesenchymal transition (EMT) pathways. AIMS: The exact cause of IPF is not fully understood and remains mysterious. It is not suppressing that non-coding RNAs are involved in the development and progression of IPF. Accordingly, here we aimed to identify non-coding RNA molecules during TGFß-induced myofibroblast activation. METHODS: Differential expression and functional enrichment analysis were employed to reveal the impact of non-coding RNAs during TGFß-associated lung fibrosis. RESULTS: Remarkably, LOC101448202, CZ1P-ASNS, LINC01503, IER3-AS1, MIR503HG, CLMAT3, LINC02593, ACTA2-AS1, LOC102723692, LOC107985728, and LOC105371064 were identified to be differentially altered during TGFß-stimulated myofibroblast activation. CONCLUSIONS: These findings strongly suggest that the mechanism of lung fibrosis is heavily under control of non-coding RNAs, and RNA-based therapies could be a promising approach for future therapeutic interventions to lung fibrosis.
ABSTRACT
Fibrosis is a pathological wound-healing mechanism that results by the overactivation of fibroblasts. Fibrosis can become obstructive and deleterious during regeneration of various body tissues including cardiac muscle. This ultimately results in the development of cardiac fibrosis, characterized by an excessive buildup of extracellular matrix proteins. Thus, it could lead to arrhythmias and heart failure which creates a leading public health burden worldwide. MiRNAs are small non-coding RNAs with great potential for diagnostic and therapeutic purposes. Mounting evidence indicates that miRNAs are involved in the deregulation of tissue homeostasis during myocardial fibrosis. For instance, miRNAs that are implicated in the regulation of TGF-beta signaling pathway have been reported to be significantly altered in myocardial fibrosis. Accordingly, in this comprehensive review, we discuss and highlight recent available data on the role of miRNAs during myocardial fibrosis, providing valuable insights into the miRNA modulation of cardiac fibrosis and miRNAs targets that can be used in the future therapeutic interventions to cardiac fibrosis.
