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您的检索式：作者名="Yunchen Luo"
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| 1 | A multi-omic landscape of steatosis-to-NASH progression显示文摘Nonalcoholic steatohepatitis(NASH)has emerged as a major cause of liver failure and hepatocellular carcinoma.Investigation into the molecular mechanisms that underlie steatosis-to-NASH progression is key to understanding the development of NASH pathophysiology.Here,we present comprehensive multi-omic profiles of preclinical animal models to identify genes,non-coding RNAs,proteins,and plasma metabolites involved in this progression.In particular,by transcriptomics analysis,we identified Growth Differentiation Factor 3(GDF3)as a candidate noninvasive biomarker in NASH.Plasma GDF3 levels are associated with hepatic pathological features in patients with NASH,and differences in these levels provide a high diagnostic accuracy of NASH diagnosis(AUROC=0.90;95%confidence interval:0.85−0.95)with a good sensitivity(90.7%)and specificity(86.4%).In addition,by developing integrated proteomic-metabolomic datasets and performing a subsequent pharmacological intervention in a mouse model of NASH,we show that ferroptosis may be a potential target to treat NASH.Moreover,by using competing endogenous RNAs network analysis,we found that several miRNAs,including miR-582-5p and miR-292a-3p,and lncRNAs,including XLOC-085738 and XLOC-041531,are associated with steatosis-to-NASH progression.Collectively,our data provide a valuable resource into the molecular characterization of NASH progression,leading to the novel insight that GDF3 may be a potential noninvasive diagnostic biomarker for NASH while further showing that ferroptosis is a therapeutic target for the disease. | Liping Xiang Xiaoyan Li Yunchen Luo Bing Zhou Yuejun Liu Yao Li Duojiao Wu Lijing Jia Pei-Wu Zhu Ming-Hua Zheng Hua Wang Yan Lu | 2022 | Life Metabolism2022，1，3： | 0 |
| 2 | Promotion of nonalcoholic steatohepatitis by RNA N^(6)-methyladenosine reader IGF2BP2 in mice显示文摘Nonalcoholic steatohepatitis(NASH)has emerged as the major cause of end-stage liver diseases.However,an incomplete understanding of its molecular mechanisms severely dampens the development of pharmacotherapies.In the present study,through systematic screening of genome-wide mRNA expression from three mouse models of hepatic inflammation and fibrosis,we identified IGF2BP2,an N6-methyladenosine modification reader,as a key regulator that promotes NASH progression in mice.Adenovirus or adeno-associated virus-mediated overexpression of IGF2BP2 could induce liver steatosis,inflammation,and fibrosis in mice,at least in part,by increasing Tab2 mRNA stability.Besides,hepatic overexpression of IGF2BP2 mimicked gene expression profiles and molecular pathways of human NASH livers.Of potential clinical significance,IGF2BP2 expression is significantly upregulated in the livers of NASH patients.Moreover,knockdown of IGF2BP2 substantially alleviated liver injury,inflammation,and fibrosis in diet-induced NASH mice.Taken together,our findings reveal an important role of IGF2BP2 in NASH,which may provide a new therapeutic target for the treatment of NASH. | Bing Zhou Yunchen Luo Nana Ji Fei Mao Liping Xiang Hua Bian Ming-Hua Zheng Cheng Hu Yao Li Yan Lu | 2022 | Life Metabolism2022，1，2： | 0 |
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