自噬对两性再现性的建设性和破坏性影响,全面综述。

IF 14.6 1区 生物学 Q1 CELL BIOLOGY
Autophagy Pub Date : 2023-12-01 Epub Date: 2023-07-28 DOI:10.1080/15548627.2023.2238577
Mohammad Samare-Najaf, Asma Neisy, Ali Samareh, Delaram Moghadam, Navid Jamali, Reza Zarei, Fatemeh Zal
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引用次数: 0

摘要

生殖的特点是在分子、细胞和组织水平上进行一系列大规模的改造。最近的研究强烈倾向于揭示生殖过程中基本分子途径的参与,如自噬,一种高度保守的真核细胞循环。这篇综述全面描述了目前关于男性生殖过程中自噬作用的知识,更新至2022年9月,包括精子发生、精子活力和活力,以及男性和女性性激素,包括生殖细胞和卵母细胞活力、排卵、植入、受精和女性性荷尔蒙。此外,还讨论了自噬流量中断对生殖障碍的影响,包括少精症、无精子症、弱精子症、畸形精子症、球精子症、卵巢早衰、多囊卵巢综合征、子宫内膜异位症和其他与不孕相关的疾病。缩写:AKT/蛋白激酶B:AKT丝氨酸/苏氨酸激酶;AMPK:AMP活化蛋白激酶;ATG:自噬相关;E2:雌激素;ED:内分泌干扰物;ER:内质网;FSH:促卵泡激素;FOX:叉头盒;GC:颗粒细胞;HIF:缺氧诱导因子;IVF:体外受精;IVM:体外成熟;LC:Leydig细胞;LDs:脂滴;LH:促黄体生成激素;LRWD1:富含亮氨酸的重复序列和含有1的WD重复结构域;MAP1LC3:微管相关蛋白1轻链3;MAPK:丝裂原活化蛋白激酶;MTOR:雷帕霉素激酶的机制靶点;NFKB/NF-kB:核因子κB;P4:黄体酮;PCOS:多囊卵巢综合征;PDLIM1:PDZ和LIM结构域1;PI3K:磷酸肌醇3-激酶;PtdIns3P:磷脂酰肌醇-3-磷酸;PtdIns3K:III类磷脂酰肌醇3-激酶;POI:卵巢早衰;ROS:活性氧;SC:支持细胞;SQSTM1/p62:螯合体1;TSGA10:睾丸特异性10;TST:睾酮;VCP:含有血管素的蛋白质。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The constructive and destructive impact of autophagy on both genders' reproducibility, a comprehensive review.

Reproduction is characterized by a series of massive renovations at molecular, cellular, and tissue levels. Recent studies have strongly tended to reveal the involvement of basic molecular pathways such as autophagy, a highly conserved eukaryotic cellular recycling, during reproductive processes. This review comprehensively describes the current knowledge, updated to September 2022, of autophagy contribution during reproductive processes in males including spermatogenesis, sperm motility and viability, and male sex hormones and females including germ cells and oocytes viability, ovulation, implantation, fertilization, and female sex hormones. Furthermore, the consequences of disruption in autophagic flux on the reproductive disorders including oligospermia, azoospermia, asthenozoospermia, teratozoospermia, globozoospermia, premature ovarian insufficiency, polycystic ovarian syndrome, endometriosis, and other disorders related to infertility are discussed as well.Abbreviations: AKT/protein kinase B: AKT serine/threonine kinase; AMPK: AMP-activated protein kinase; ATG: autophagy related; E2: estrogen; EDs: endocrine disruptors; ER: endoplasmic reticulum; FSH: follicle stimulating hormone; FOX: forkhead box; GCs: granulosa cells; HIF: hypoxia inducible factor; IVF: in vitro fertilization; IVM: in vitro maturation; LCs: Leydig cells; LDs: lipid droplets; LH: luteinizing hormone; LRWD1: leucine rich repeats and WD repeat domain containing 1; MAP1LC3: microtubule associated protein 1 light chain 3; MAPK: mitogen-activated protein kinase; MTOR: mechanistic target of rapamycin kinase; NFKB/NF-kB: nuclear factor kappa B; P4: progesterone; PCOS: polycystic ovarian syndrome; PDLIM1: PDZ and LIM domain 1; PI3K: phosphoinositide 3-kinase; PtdIns3P: phosphatidylinositol-3-phosphate; PtdIns3K: class III phosphatidylinositol 3-kinase; POI: premature ovarian insufficiency; ROS: reactive oxygen species; SCs: Sertoli cells; SQSTM1/p62: sequestosome 1; TSGA10: testis specific 10; TST: testosterone; VCP: vasolin containing protein.

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来源期刊
Autophagy
Autophagy 生物-细胞生物学
CiteScore
21.30
自引率
2.30%
发文量
277
审稿时长
1 months
期刊介绍: Autophagy is a peer-reviewed journal that publishes research on autophagic processes, including the lysosome/vacuole dependent degradation of intracellular material. It aims to be the premier journal in the field and covers various connections between autophagy and human health and disease, such as cancer, neurodegeneration, aging, diabetes, myopathies, and heart disease. Autophagy is interested in all experimental systems, from yeast to human. Suggestions for specialized topics are welcome. The journal accepts the following types of articles: Original research, Reviews, Technical papers, Brief Reports, Addenda, Letters to the Editor, Commentaries and Views, and Articles on science and art. Autophagy is abstracted/indexed in Adis International Ltd (Reactions Weekly), EBSCOhost (Biological Abstracts), Elsevier BV (EMBASE and Scopus), PubMed, Biological Abstracts, Science Citation Index Expanded, Web of Science, and MEDLINE.
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