Lambda-cyhalothrin induces lipid accumulation in mouse liver is associated with AMPK inactivation

Yang, Daqian; Sun, Xiaotong; Wei, Xiangjuan; Zhang, Boya; Fan, Xingpei; Du, Hai-Ning; Zhu, Ruijiao; Oh, Yuri; Gu, Ning

doi:10.1016/j.fct.2022.113563

Cited by 5 publications

(2 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…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%

“…AMPK signaling pathway could reduce alcohol-induced liver injury and enhance hepatocyte mitophagy level [48]. The activation of AMPK in hepatocytes effectively attenuated the effects of lambda-cyhalothrin-induced hepatic steatosis [49]. In addition, AMPK signaling pathway was linked to the effects of ferulic acid in upregulating the hepatic speci c markers (HNF4a, Foxa2, and Alb) [50].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Unveiling the Hub Genes Associated with Manganese-Induced Hepatotoxicity

Yang

Wang

et al. 2023

Preprint

View full text Add to dashboard Cite

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.

show abstract