Mitochondrial dysfunction: A promising therapeutic target for liver diseases

Chen, Ping; Yao, Lichao; Yuan, Mengqin; Wang, Zheng; Zhang, Qiuling; Jiang, Yingan; Li, Lanjuan

doi:10.1016/j.gendis.2023.101115

Cited by 14 publications

(2 citation statements)

References 144 publications

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“…The depletion of GSH and increase in GSSG levels indicate a decrease in the intracellular ability to clear lipid peroxides, leading to ferroptosis. Oxidative stress causes cell ferroptosis, which can lead to mitochondrial damage, resulting in the reduction or disappearance of mitochondrial cristae and a decrease in mitochondrial membrane potential [25]. In the current study, a decrease in mitochondrial membrane potential induced by erastin was detected.…”

Section: Discussionsupporting

confidence: 51%

circAMN1-Mediated Ferroptosis Regulates the Expulsion of Placenta in Trophoblast Cells

Lv,

Guo,

Wang

et al. 2024

Antioxidants

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After delivery, the death of trophoblast cells can promote the expulsion of the placenta. Ferroptosis, an iron-dependent programmed cell death, is involved in mammalian development. Circular RNAs are associated with placental development; however, it is unclear whether circular RNAs regulate the expulsion of fetal membranes through ferroptosis. The gene expression profiles in the tail vein blood of Holstein cows with normal and retained placentas were investigated using RNA sequencing and a GSE214588 dataset. circAMN1 and SLC39A8 expression was significantly downregulated in the blood of cows with a retained placenta, whereas miR-205_R-1 expression was significantly upregulated. We validated erastin-induced ferroptosis in trophoblast cells. Transfection with si-circAMN1 and miR-205_R-1 mimic reduced intracellular total iron, Fe2+, and glutathione disulfide levels; increased intracellular glutathione levels and glutathione/glutathione disulfide; and enhanced cell viability in these cells. In contrast, transfection with pcDNA3.1 circAMN1 and an miR-205_R-1 inhibitor promoted ferroptosis. As an miR-205_R-1 sponge, circAMN1 regulated the expression of SLC39A8 to control erastin-induced ferroptosis and regulated the proliferation, invasion, and migration of trophoblast cells. Our findings provide a theoretical basis for studying the mechanism by which programmed cell death regulates fetal membrane expulsion and indicate its potential as a therapeutic target for placenta retention.

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