id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
cord-344960-m1spgpyu	Liu, Ying	Roles of MicroRNA-122 in Cardiovascular Fibrosis and Related Diseases	2020-08-27		.txt	text/plain	5034	270	33	MiR-122 overexpression appears to exacerbate the angiotensin II-mediated loss of autophagy and increased inflammation, apoptosis, extracellular matrix deposition, cardiovascular fibrosis and dysfunction by modulating the SIRT6-Elabela-ACE2, LGR4-β-catenin, TGFβ-CTGF and PTEN-PI3K-Akt signaling pathways. We previously demonstrated that miR-122 overexpression exacerbated the loss of autophagy and increased cellular migration, apoptosis, extracellular matrix deposition mediated by angiotensin II by modulating the SIRT6-ELA-ACE2, leucine-rich repeat-containing G-protein-coupled receptors 4 (LGR4)-β-catenin, and TGFβ-CTGF signaling pathways (Table 1 ; Fig. 3 ) [1, 6] , indicating that miR-122 inhibition is a promising therapeutic strategy for cardiac fibrosis and dysfunction. Our previous study demonstrated that administration of a miR-122 inhibitor effectively prevented the loss of autophagy and increased cellular proliferation, migration, apoptosis and cardiovascular fibrosis induced by Ang II via modulation of the SIRT6-ELA-ACE2, LGR4/β-catenin and TGFβ1-CTGF-NFAT5 signaling pathways (Table 1 ; Fig. 3 ) [1, 6] .	./cache/cord-344960-m1spgpyu.txt	./txt/cord-344960-m1spgpyu.txt