Dapagliflozin Presented Nonalcoholic Fatty Liver Through Metabolite
                    Extraction and AMPK/NLRP3 Signaling Pathway

Deng, Lin; Song, Yiyun

doi:10.1055/a-1970-3388

Cited by 4 publications

(2 citation statements)

References 36 publications

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“…In the present study, the DEGs in the livers between treated with and without MnCl 2 on the 3rd and 5th day were involved in AMPK signaling pathway (Fig. 3B-C), which was consistent with previous ndings [47][48][49][50]. AMPK signaling pathway induced by dapagli ozin reduced oxidative stress and in ammation in vitro model of NAFLD [47].…”

Section: Discussionsupporting

confidence: 92%

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Unveiling the Hub Genes Associated with Manganese-Induced Hepatotoxicity

Yang

Wang

et al. 2023

Preprint

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Excessive exposure to manganese (Mn) can cause severe toxicity in human and animal organs, particularly the liver. However, the specific mechanisms of Mn-induced hepatotoxicity remain unclear. Thus, the objective of this study was to identify the key genes associated with hepatotoxicity caused by Mn administration. We obtained the gene expression data set GSE59923 from the Gene Expression Omnibus, which included liver samples treated with manganese chloride (MnCl2) as well as control samples. Through our analysis, we identified 222, 351, and 494 differentially expressed genes (DEGs) in the livers treated with MnCl2 at 700 mg/kg on the 1st, 3rd, and 5th day, respectively. Notably, we found a total of 27 overlapping DEGs in the liver samples. Biological process analysis revealed that these common DEGs were associated with the response to xenobiotic stimulus, cellular calcium ion homeostasis, and ion transmembrane transport. Pathway analysis further indicated the involvement of cAMP, p53, PI3K-Akt, MAPK, and AMPK signaling pathways in Mn-induced hepatotoxicity. Furthermore, we identified several important genes, including CCR2, CDKN1A, CELSR2, LCN2, and PER2, which appeared to play a role in Mn-induced hepatotoxicity. Taken together, this study sheds light on the molecular mechanisms underlying Mn-induced hepatotoxicity, contributing to our overall understanding of this condition.

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Section: Discussionsupporting

confidence: 92%

“…3B-C), which was consistent with previous ndings [47][48][49][50]. AMPK signaling pathway induced by dapagli ozin reduced oxidative stress and in ammation in vitro model of NAFLD [47]. AMPK signaling pathway could reduce alcohol-induced liver injury and enhance hepatocyte mitophagy level [48].…”

Section: Discussionsupporting

confidence: 90%