Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive and devastating disorder. It is characterized by alveolar epithelial cell injury and activation, infiltration of inflammatory cells, initiation of epithelial mesenchymal transition (EMT), aberrant proliferation and activation of fibroblasts, exaggerated deposition of extracellular matrix (ECM) proteins, and finally leading to the destruction of lung parenchyma. MicroRNAs (miRNAs) are endogenous small non-coding RNA molecules that post-transcriptionally regulate gene expression in diverse biological and pathological processes, including cell proliferation, differentiation, apoptosis and metastasis. As a result, miRNAs have emerged as a major area of biomedical research with relevance to pulmonary fibrosis. In this context, the present review discusses specific patterns of dysregulated miRNAs in patients with IPF. Further, we discuss the current understanding of miRNAs involvement in regulating lung inflammation, TGF-β1-mediated EMT and fibroblast differentiation processes, ECM genes expression, and in the progression of lung fibrosis. The possible future directions that might lead to novel therapeutic strategies for the treatment of pulmonary fibrosis are also reviewed.
A sequential anaerobic aerobic treatment process based on mixed culture of bacteria isolated from textile dye effluent-contaminated soil was used to degrade sulfonated azo dyes Orange G (OG), Amido black 10B (AB), Direct red 4BS (DR) and Congo red (CR). Under anaerobic conditions in a fixed-bed column using glucose as co-substrate, the azo dyes were reduced and amines were released by the bacterial biomass. The amines were completely mineralized in a subsequent aerobic treatment using the same isolates. The maximum degradation rate observed in the treatment system for OG was 60.9 mg/l per day (16.99 mg/g glucose utilized), for AB 571.3 mg/l per day (14.46 mg/g glucose utilized), for DR 112.5 mg/l per day (32.02 mg/g glucose utilized) and for CR 134.9 mg/l per day (38.9 mg/g glucose utilized).
Collectively, our findings indicate the therapeutic potential of Nrf2 activation by PTS as a promising approach to safeguard pancreatic beta-cells against oxidative damage in diabetes.
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