“…Treatment of a currently clinical-trialed DN drug, Atrasentan (an endothelin-1 receptor antagonist) reduced miR-21 expression, restored the Foxo1 expression, and thus promoted renal autophagy (Wang et al, 2019a). Therefore, following TGFB response, majority of these downstream network of miRNA activates the PI3K/AKT/mTOR pathway, by targeting the PTEN (miR-216a, miR-217, miR-21, miR-22, miR-25, and miR-214) (Kato et al, 2009;Denby et al, 2011;Li et al, 2017a;, collagen type I alpha1 (COLIA1), Collagen IV (COL4), and Fibronectin (FN) (miR-130b) (Ma et al, 2019), PI3K inhibitor (Fog2) (miR-200 family) (Park et al, 2013), Tyrosine 3monooxygenase (Ywhab) (miR-451) (Zhang et al, 2012), DEP domain-containing mTOR-interacting protein (Deptor) (miR-181a) (Maity et al, 2018), Protein canopy homolog-1 (Cnpy1) (miR-370) (Yu et al, 2019), high−mobility group AT−hook-2, Hmga2 (let-7a-5p) (Wang et al, 2019c), Insulin receptor substrate-2, IRS2 (miR-141) (Li et al, 2018b), forkhead box proteins, and Foxo1 (miR-382) (Wang et al, 2018c) genes. Some of these miRNAs are found in circulating bio-fluids and therefore, could potentially be as biomarkers.…”