2018
DOI: 10.1016/j.orcp.2018.06.005
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MiR-122 marks the differences between subcutaneous and visceral adipose tissues and associates with the outcome of bariatric surgery

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Cited by 26 publications
(30 citation statements)
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“…Recent research has shown that miR-122 overexpression induces hepatic differentiation of adipose tissue-derived stem cells [51]. In addition, miR-122 is also the most significant signature between visceral fat and subcutaneous fat, and its abundance affects PPAR-γ signalling and adipocyte differentiation in vitro and in human adipose tissues [52]. Although the function of miR-499 in lipid metabolism has not been reported, a recent study has shown that miR-499 can regulate PRDM16 to affect insulin-induced skeletal muscle satellite cell (SMSC) adipogenic differentiation [53].…”
Section: Discussionmentioning
confidence: 99%
“…Recent research has shown that miR-122 overexpression induces hepatic differentiation of adipose tissue-derived stem cells [51]. In addition, miR-122 is also the most significant signature between visceral fat and subcutaneous fat, and its abundance affects PPAR-γ signalling and adipocyte differentiation in vitro and in human adipose tissues [52]. Although the function of miR-499 in lipid metabolism has not been reported, a recent study has shown that miR-499 can regulate PRDM16 to affect insulin-induced skeletal muscle satellite cell (SMSC) adipogenic differentiation [53].…”
Section: Discussionmentioning
confidence: 99%
“…MiRs participate in regulating cell proliferation, migration, differentiation, and apoptosis and function as crucial determinants and biomarkers of cardiovascular fibrosis [1,5,6,30,32]. In particular, miR-122 has been implicated in the progression of fibrosis and acts as a circulatory biomarker in hypertension and HF [1,6,17,18,[33][34][35][36][37]. 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.…”
Section: Mir-122 and Cardiovascular Fibrosis And Remodelingmentioning
confidence: 99%
“…miR-122 is another candidate miRNA because it is downregulated in the liver in fructose-fed rats [132]. This miRNA suppresses PPARγ expression in 3T3-L1 preadipocytes [133]. Induction of miR-378a can also be involved.…”
Section: Micrornas Implication In Fructose-induced Adipogenesismentioning
confidence: 99%