Role of miRNA and lncRNAs in organ fibrosis and aging

Fibrosis is the endpoint of pathological remodeling. This process contributes to the pathogenesis of several chronic disorders and aging-associated organ damage. Different molecular cascades contribute to this process. TGF-β, WNT, and YAP/TAZ signaling pathways have prominent roles in this process. A number of long non-coding RNAs and microRNAs have been found to regulate organ fibrosis through modulation of the activity of related signaling pathways. miR-144-3p, miR-451, miR-200b, and miR-328 are among microRNAs that participate in the pathology of cardiac fibrosis. Meanwhile, miR-34a, miR-17-5p, miR-122, miR-146a, and miR-350 contribute to liver fibrosis in different situations. PVT1, MALAT1, GAS5, NRON, PFL, MIAT, HULC, ANRIL, and H19 are among long non-coding RNAs that participate in organ fibrosis. We review the impact of long non-coding RNAs and microRNAs in organ fibrosis and aging-related pathologies

Interaction between non-coding RNAs and Toll-like receptors

Toll-like receptors (TLRs) are a large group of pattern recognition receptors which are involved in the regulation of innate immune responses. Based on the interplay between TLRs and adapter molecules, two distinctive signaling cascades, namely the MyD88-dependent and TRIF-dependent pathways have been recognized. TLRs are involved in the development of a wide variety of diseases including cancer and autoimmune disorders. A large body of evidence has shown interaction between two classes of non-coding RNAs, namely microRNAs (miRNAs) and long noncoding RNAs (lncRNAs). These interactions have prominent roles in the pathogenesis of several disorders including infectious disorders, autoimmune conditions and neoplastic disorders. This review aims at description of the interaction between these non-coding RNAs and TLRs