<i>Epg5</i> deficiency leads to primary ovarian insufficiency due to WT1 accumulation in mouse granulosa cells

Liu, Wenwen; Chen, Min; Liu, Chao; Wang, Liying; Wei, Haixia; Zhang, Ruidan; Ren, Zhengxing; Chen, Yinghong; Luo, Mengcheng; Zhao, Jianguo; Jiang, Hongwei; Gao, Fei; Li, Wei

doi:10.1080/15548627.2022.2094671

Cited by 28 publications

(19 citation statements)

References 74 publications

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“…43 In this study, our results after CQ intervention were consistent with the study results of Liu et al, showing that the expression of LC3II protein increased. 44 The activation process of HSCs can be reversed and liver fibrosis can be alleviated through the inhibition of autophagy. 45 This is consistent with our study results.…”

Section: Discussionmentioning

confidence: 99%

Lysine specific demethylase 1 inhibits sodium arsenite activation of HSCs by regulating SESN2/AMPK/ULK1 signaling pathway activity

Zhang,

Tian,

Liang

et al. 2024

Environmental Toxicology

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Lysine specific demethylase 1 (LSD1) is a histone demethylase that specifically catalyzes the demethylation of histone H3K4 (H3K4me1/2) and regulates gene expression. In addition, it can mediate the process of autophagy through its demethylase activity. Sestrin2 (SESN2) is a stress‐induced protein and a positive regulator of autophagy. In NaAsO2‐induced mouse fibrotic livers and activated hepatic stellate cells (HSCs), LSD1 expression is decreased, SESN2 expression is increased, and autophagy levels are also increased. Overexpression of LSD1 and silencing of SESN2 decreased the level of autophagy and attenuated the activation of HSCs induced by NaAsO2. LSD1 promoted SESN2 gene transcription by increasing H3K4me1/2 in the SESN2 promoter region. 3‐methyladenine (3‐MA) and chloroquine were used to inhibit autophagy of HSCs, and the degree of activation was also alleviated. Taken together, LSD1 positively regulates SESN2 by increasing H3K4me1/2 enrichment in the SESN2 promoter region, which in turn increases the level of autophagy and promotes the activation of HSCs. Our results may provide new evidence for the importance of LSD1 in the process of autophagy and activation of HSCs induced by arsenic poisoning. Increasing the expression and activity of LSD1 is expected to be an effective way to reverse the autophagy and activation of HSCs induced by arsenic poisoning.

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Section: Discussionmentioning

confidence: 99%

Lysine specific demethylase 1 inhibits sodium arsenite activation of HSCs by regulating SESN2/AMPK/ULK1 signaling pathway activity

Zhang,

Tian,

Liang

et al. 2024

Environmental Toxicology

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“…Inhibition of autophagy leads to the accumulation of WT1 protein in granulosa cells, which decreases the levels of cytochrome P450 family 19 subfamily A member 1 and FSHR, resulting in the disruption of granulosa cell differentiation [ 22 ]. For the regulation of WT1, Epg5 ( ectopic P-granules 5 autophagy tethering factor ), whose deleted mice showed a phenotype similar to that of patients with premature ovarian failure, promotes WT1 degradation via p62 in granulosa cells [ 24 ]. Senescent and apoptotic cells increase with aging.…”

Section: Role Of Autophagy In Ovarian Functionsmentioning

confidence: 99%

The Role of Autophagy in the Female Reproduction System: For Beginners to Experts in This Field

Nakashima

Furuta

Yamada

et al. 2023

Biology

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Autophagy is a fundamental process involved in regulating cellular homeostasis. Autophagy has been classically discovered as a cellular process that degrades cytoplasmic components non-selectively to produce energy. Over the past few decades, this process has been shown to work in energy production, as well as in the reduction of excessive proteins, damaged organelles, and membrane trafficking. It contributes to many human diseases, such as neurodegenerative diseases, carcinogenesis, diabetes mellitus, development, longevity, and reproduction. In this review, we provide important information for interpreting results related to autophagic experiments and present the role of autophagy in this field.

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“…Niedawno opublikowane badanie wyjaśnia wpływ LncRNA na patogenezę POI [24]. Dzięki coraz szerszemu poznaniu mutacji odpowiedzialnych za wystąpienie POI możliwe jest badanie określonych szlaków komórkowych, mających wpływ na funkcjonowanie jajnika [25].…”

Section: Przyczynyunclassified

Premature Ovarian Insufficiency - diagnostic and therapeutic challenges

HAWRANIK

TOMASIK

WARZYSZAK

et al. 2023

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Introduction and purpose: Premature Ovarian Insufficiency (POI) is a rare but serious disease diagnosed in about 1% of women before the age of 40. It is characterized by hypoestrogenism and an increase in the level of the follicle-stimulating hormone, which is associated with menstrual disorders, pregnancy failures and a reduced quality of life. The main causes of POI include a genetic background and autoimmune abnormalities, as well as increasingly jatrogenic factors. Care for patients is focused on hormone replacement therapy and infertility treatment. The aim of this review is to discuss current treatment methods, the impact of early diagnosis and the prevention of premature ovarian insufficiency, which affects the ability to have one's own offspring. The article also describes new methods of infertility treatment that are under investigation. Materials and methods: This literature review is based on articles published in the PubMed database from 2015 to 2022 using the following phrases: premature ovarian insufficiency, premature ovarian insufficiency stem cells State of knowledge: The only way to treat infertility in women with POI is egg donation. Currently, research is being conducted to achieve early diagnosis, introduce new treatment methods and reduce the number of iatrogenic forms of POI. Conclusion: The main problem for women diagnosed with POI is the difficulty or often impossibility of having their own children. Egg donation does not allow for the transfer of the patient's genetic material, and is also not available as a treatment option in some countries. For this reason, new methods for early diagnosis, treatment, and prevention of POI are being developed.

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Epg5 deficiency leads to primary ovarian insufficiency due to WT1 accumulation in mouse granulosa cells

Cited by 28 publications

References 74 publications

Lysine specific demethylase 1 inhibits sodium arsenite activation of HSCs by regulating SESN2/AMPK/ULK1 signaling pathway activity

Lysine specific demethylase 1 inhibits sodium arsenite activation of HSCs by regulating SESN2/AMPK/ULK1 signaling pathway activity

The Role of Autophagy in the Female Reproduction System: For Beginners to Experts in This Field

Premature Ovarian Insufficiency - diagnostic and therapeutic challenges

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