Cellular and Molecular Life Sciences最新文献_第8页

Correction: A novel Bacillus aerolatus CX253 attenuates inflammation induced by Streptococcus pneumoniae in childhood and pregnant rats by regulating gut microbiome. 更正：新型气溶胶芽孢杆菌 CX253 可通过调节肠道微生物群减轻肺炎链球菌诱发的儿童和怀孕大鼠炎症。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2024-09-10 DOI: 10.1007/s00018-024-05405-x

Ting Yu, Biru Wu, Dimei Zhang, Guanhua Deng, Yi Luo, Ningqianzi Tang, Qiankun Shi, Fang Hu, Guoxia Zhang

引用次数: 0

Neurobiological research on N,N-dimethyltryptamine (DMT) and its potentiation by monoamine oxidase (MAO) inhibition: from ayahuasca to synthetic combinations of DMT and MAO inhibitors 关于 N,N-二甲基色胺（DMT）及其单胺氧化酶（MAO）抑制增效作用的神经生物学研究：从死藤水到 DMT 和 MAO 抑制剂的合成组合物

IF 8 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2024-09-10 DOI: 10.1007/s00018-024-05353-6

Klemens Egger, Helena D. Aicher, Paul Cumming, Milan Scheidegger

{"title":"Neurobiological research on N,N-dimethyltryptamine (DMT) and its potentiation by monoamine oxidase (MAO) inhibition: from ayahuasca to synthetic combinations of DMT and MAO inhibitors","authors":"Klemens Egger, Helena D. Aicher, Paul Cumming, Milan Scheidegger","doi":"10.1007/s00018-024-05353-6","DOIUrl":"https://doi.org/10.1007/s00018-024-05353-6","url":null,"abstract":"The potent hallucinogen N,N-dimethyltryptamine (DMT) has garnered significant interest in recent years due to its profound effects on consciousness and its therapeutic psychopotential. DMT is an integral (but not exclusive) psychoactive alkaloid in the Amazonian plant-based brew ayahuasca, in which admixture of several β-carboline monoamine oxidase A (MAO-A) inhibitors potentiate the activity of oral DMT, while possibly contributing in other respects to the complex psychopharmacology of ayahuasca. Irrespective of the route of administration, DMT alters perception, mood, and cognition, presumably through agonism at serotonin (5-HT) 1A/2A/2C receptors in brain, with additional actions at other receptor types possibly contributing to its overall psychoactive effects. Due to rapid first pass metabolism, DMT is nearly inactive orally, but co-administration with β-carbolines or synthetic MAO-A inhibitors (MAOIs) greatly increase its bioavailability and duration of action. The synergistic effects of DMT and MAOIs in ayahuasca or synthetic formulations may promote neuroplasticity, which presumably underlies their promising therapeutic efficacy in clinical trials for neuropsychiatric disorders, including depression, addiction, and post-traumatic stress disorder. Advances in neuroimaging techniques are elucidating the neural correlates of DMT-induced altered states of consciousness, revealing alterations in brain activity, functional connectivity, and network dynamics. In this comprehensive narrative review, we present a synthesis of current knowledge on the pharmacology and neuroscience of DMT, β-carbolines, and ayahuasca, which should inform future research aiming to harness their full therapeutic potential.","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"64 1","pages":""},"PeriodicalIF":8.0,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142218260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Correction: A novel gene-trap line reveals the dynamic patterns and essential roles of cysteine and glycine-rich protein 3 in zebrafish heart development and regeneration 更正：新型基因诱捕系揭示了半胱氨酸和富含甘氨酸的蛋白 3 在斑马鱼心脏发育和再生过程中的动态模式和重要作用

IF 8 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2024-09-10 DOI: 10.1007/s00018-024-05334-9

Shuzhang Liang, Yating Zhou, Yue Chang, Jiayi Li, Min Zhang, Peng Gao, Qi Li, Hong Yu, Koichi Kawakami, Jinmin Ma, Ruilin Zhang

引用次数: 0

Epitranscriptomic regulation of lipid oxidation and liver fibrosis via ENPP1 mRNA m⁶A modification. 通过 ENPP1 mRNA m6A 修饰调控脂质氧化和肝纤维化的外显子转录组。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2024-09-09 DOI: 10.1007/s00018-024-05420-y

Feng Sun, Juan Wang, Yang Yang, Qi-Qi Dong, Lin Jia, Wei Hu, Hui Tao, Chao Lu, Jing-Jing Yang

{"title":"Epitranscriptomic regulation of lipid oxidation and liver fibrosis via ENPP1 mRNA m6A modification.","authors":"Feng Sun, Juan Wang, Yang Yang, Qi-Qi Dong, Lin Jia, Wei Hu, Hui Tao, Chao Lu, Jing-Jing Yang","doi":"10.1007/s00018-024-05420-y","DOIUrl":"10.1007/s00018-024-05420-y","url":null,"abstract":"Background: Dysregulated lipid oxidation occurs in several pathological processes characterized by cell proliferation and migration. Nonetheless, the molecular mechanism of lipid oxidation is not well appreciated in liver fibrosis, which is accompanied by enhanced fibroblast proliferation and migration.Methods: We investigated the causes and consequences of lipid oxidation in liver fibrosis using cultured cells, animal models, and clinical samples.Results: Increased ecto-nucleotide pyrophosphatase/phosphodiesterase (ENPP1) expression caused increased lipid oxidation, resulting in the proliferation and migration of hepatic stellate cells (HSCs) that lead to liver fibrosis, whereas fibroblast-specific ENPP1 knockout reversing these results. Elevated ENPP1 and N6-methyladenosine (m6A) levels were associated with high expression of Wilms tumor 1 associated protein (WTAP). Mechanistically, WTAP-mediated m6A methylation of the 3'UTR of ENPP1 mRNA and induces its translation dependent of YTH domain family proteins 1 (YTHDF1). Additionally, ENPP1 could interact with hypoxia inducible lipid droplet associated (HILPDA) directly; overexpression of ENPP1 further recruits HILPDA-mediated lipid oxidation, thereby promotes HSCs proliferation and migration, while inhibition of ENPP1 expression produced the opposite effect. Clinically, increased expression of WTAP, YTHDF1, ENPP1, and HILPDA, and increased m6A mRNA content, enhanced lipid oxidation, and increased collagen deposition in human liver fibrosis tissues.Conclusions: We describe a novel mechanism in which WTAP catalyzes m6A methylation of ENPP1 in a YTHDF1-dependent manner to enhance lipid oxidation, promoting HSCs proliferation and migration and liver fibrosis.","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"81 1","pages":"387"},"PeriodicalIF":6.2,"publicationDate":"2024-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11383905/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142153236","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Human coronaviruses activate and hijack the host transcription factor HSF1 to enhance viral replication. 人类冠状病毒激活并劫持宿主转录因子 HSF1，以加强病毒复制。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2024-09-07 DOI: 10.1007/s00018-024-05370-5

Silvia Pauciullo, Anna Riccio, Silvia Santopolo, Anna Albecka, Guido Papa, Leo C James, Sara Piacentini, Giulia Lanzilli, Antonio Rossi, M Gabriella Santoro

{"title":"Human coronaviruses activate and hijack the host transcription factor HSF1 to enhance viral replication.","authors":"Silvia Pauciullo, Anna Riccio, Silvia Santopolo, Anna Albecka, Guido Papa, Leo C James, Sara Piacentini, Giulia Lanzilli, Antonio Rossi, M Gabriella Santoro","doi":"10.1007/s00018-024-05370-5","DOIUrl":"10.1007/s00018-024-05370-5","url":null,"abstract":"Organisms respond to proteotoxic-stress by activating the heat-shock response, a cellular defense mechanism regulated by a family of heat-shock factors (HSFs); among six human HSFs, HSF1 acts as a proteostasis guardian regulating severe stress-driven transcriptional responses. Herein we show that human coronaviruses (HCoV), both low-pathogenic seasonal-HCoVs and highly-pathogenic SARS-CoV-2 variants, are potent inducers of HSF1, promoting HSF1 serine-326 phosphorylation and triggering a powerful and distinct HSF1-driven transcriptional-translational response in infected cells. Despite the coronavirus-mediated shut-down of the host translational machinery, selected HSF1-target gene products, including HSP70, HSPA6 and AIRAP, are highly expressed in HCoV-infected cells. Using silencing experiments and a direct HSF1 small-molecule inhibitor we show that, intriguingly, HCoV-mediated activation of the HSF1-pathway, rather than representing a host defense response to infection, is hijacked by the pathogen and is essential for efficient progeny particles production. The results open new scenarios for the search of innovative antiviral strategies against coronavirus infections.","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"81 1","pages":"386"},"PeriodicalIF":6.2,"publicationDate":"2024-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11380654/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142145245","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

PARVB deficiency alleviates cisplatin-induced tubular injury by inhibiting TAK1 signaling. PARVB 缺乏可通过抑制 TAK1 信号转导减轻顺铂诱导的肾小管损伤。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2024-09-05 DOI: 10.1007/s00018-024-05422-w

Aihua Yang, Yanyan Ding, Chen Guo, Chengmin Liu, Zailin Xiong, Meiling Quan, Panzhu Bai, Renwei Cai, Binbin Li, Guizhen Li, Yi Deng, Chuanyue Wu, Ying Sun

{"title":"PARVB deficiency alleviates cisplatin-induced tubular injury by inhibiting TAK1 signaling.","authors":"Aihua Yang, Yanyan Ding, Chen Guo, Chengmin Liu, Zailin Xiong, Meiling Quan, Panzhu Bai, Renwei Cai, Binbin Li, Guizhen Li, Yi Deng, Chuanyue Wu, Ying Sun","doi":"10.1007/s00018-024-05422-w","DOIUrl":"10.1007/s00018-024-05422-w","url":null,"abstract":"Cisplatin-induced renal tubular injury largely restricts the wide-spread usage of cisplatin in the treatment of malignancies. Identifying the key signaling pathways that regulate cisplatin-induced renal tubular injury is thus clinically important. PARVB, a focal adhesion protein, plays a crucial role in tumorigenesis. However, the function of PARVB in kidney disease is largely unknown. To investigate whether and how PARVB contributes to cisplatin-induced renal tubular injury, a mouse model (PARVB cKO) was generated in which PARVB gene was specifically deleted from proximal tubular epithelial cells using the Cre-LoxP system. In this study, we found depletion of PARVB in proximal tubular epithelial cells significantly attenuates cisplatin-induced renal tubular injury, including tubular cell death and inflammation. Mechanistically, PARVB associates with transforming growth factor-β-activated kinase 1 (TAK1), a central regulator of cell survival and inflammation that is critically involved in mediating cisplatin-induced renal tubular injury. Depletion of PARVB promotes cisplatin-induced TAK1 degradation, inhibits TAK1 downstream signaling, and ultimately alleviates cisplatin-induced tubular cell damage. Restoration of PARVB or TAK1 in PARVB-deficient cells aggravates cisplatin-induced tubular cell injury. Finally, we demonstrated that PARVB regulates TAK1 protein expression through an E3 ligase ITCH-dependent pathway. PARVB prevents ITCH association with TAK1 to block its ubiquitination. Our study reveals that PARVB deficiency protects against cisplatin-induced tubular injury through regulation of TAK1 signaling and indicates targeting this pathway may provide a novel therapeutic strategy to alleviate cisplatin-induced kidney damage.","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"81 1","pages":"385"},"PeriodicalIF":6.2,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11377400/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142131988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Suppression of neuronal CDK9/p53/VDAC signaling provides bioenergetic support and improves post-stroke neuropsychiatric outcomes. 抑制神经元 CDK9/p53/VDAC 信号传导可提供生物能量支持，改善中风后的神经精神状况。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2024-09-05 DOI: 10.1007/s00018-024-05428-4

Jing Xia, Tingting Zhang, Ying Sun, Zhu Huang, Dingfang Shi, Dongshen Qin, Xuejun Yang, Hao Liu, Guiying Yao, Libin Wei, Xiaoai Chang, Jun Gao, Yongjian Guo, Xiao-Yu Hou

{"title":"Suppression of neuronal CDK9/p53/VDAC signaling provides bioenergetic support and improves post-stroke neuropsychiatric outcomes.","authors":"Jing Xia, Tingting Zhang, Ying Sun, Zhu Huang, Dingfang Shi, Dongshen Qin, Xuejun Yang, Hao Liu, Guiying Yao, Libin Wei, Xiaoai Chang, Jun Gao, Yongjian Guo, Xiao-Yu Hou","doi":"10.1007/s00018-024-05428-4","DOIUrl":"10.1007/s00018-024-05428-4","url":null,"abstract":"Bioenergy decline occurs with reperfusion following acute ischemic stroke. However, the molecular mechanisms that limit energy metabolism and their impact on post-stroke cognitive and emotional complications are still unclear. In the present study, we demonstrate that the p53 transcriptional response is responsible for neuronal adenosine triphosphate (ATP) deficiency and progressively neuropsychiatric disturbances, involving the downregulation of mitochondrial voltage-dependent anion channels (VDACs). Neuronal p53 transactivated the promoter of microRNA-183 (miR-183) cluster, thereby upregulating biogenesis of miR-183-5p (miR-183), miR-96-5p (miR-96), and miR-182-5p. Both miR-183 and miR-96 directly targeted and post-transcriptionally suppressed VDACs. Neuronal ablation of p53 protected against ATP deficiency and neurological deficits, whereas post-stroke rescue of miR-183/VDAC signaling reversed these benefits. Interestingly, cyclin-dependent kinase 9 (CDK9) was found to be enriched in cortical neurons and upregulated the p53-induced transcription of the miR-183 cluster in neurons after ischemia. Post-treatment with the CDK9 inhibitor oroxylin A promoted neuronal ATP production mainly through suppressing the miR-183 cluster/VDAC axis, further improved long-term sensorimotor abilities and spatial memory, and alleviated depressive-like behaviors in mice following stroke. Our findings reveal an intrinsic CDK9/p53/VDAC pathway that drives neuronal bioenergy decline and underlies post-stroke cognitive impairment and depression, thus highlighting the therapeutic potential of oroxylin A for better outcomes.","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"81 1","pages":"384"},"PeriodicalIF":6.2,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11377386/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142131989","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

G protein selectivity profile of GPR56/ADGRG1 and its effect on downstream effectors. GPR56/ADGRG1 的 G 蛋白选择性特征及其对下游效应物的影响。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2024-09-04 DOI: 10.1007/s00018-024-05416-8

Raida Jallouli, Ana L Moreno-Salinas, Andréanne Laniel, Brian Holleran, Charlotte Avet, Joan Jacob, Trang Hoang, Christine Lavoie, Kendra S Carmon, Michel Bouvier, Richard Leduc

{"title":"G protein selectivity profile of GPR56/ADGRG1 and its effect on downstream effectors.","authors":"Raida Jallouli, Ana L Moreno-Salinas, Andréanne Laniel, Brian Holleran, Charlotte Avet, Joan Jacob, Trang Hoang, Christine Lavoie, Kendra S Carmon, Michel Bouvier, Richard Leduc","doi":"10.1007/s00018-024-05416-8","DOIUrl":"10.1007/s00018-024-05416-8","url":null,"abstract":"GPR56, an adhesion G-protein coupled receptor (aGPCRs) with constitutive and ligand-promoted activity, is involved in many physiological and pathological processes. Whether the receptor's constitutive or ligand-promoted activation occur through the same molecular mechanism, and whether different activation modes lead to functional selectivity between G proteins is unknown. Here we show that GPR56 constitutively activates both G12 and G13. Unlike constitutive activation and activation with 3-α-acetoxydihydrodeoxygedunin (3αDOG), stimulation with an antibody, 10C7, directed against GPR56's extracellular domain (ECD) led to an activation that favors G13 over G12. An autoproteolytically deficient mutant, GPR56-T383A, was also activated by 10C7 indicating that the tethered agonist (TA) exposed through autocatalytic cleavage, is not required for this activation modality. In contrast, this proteolysis-resistant mutant could not be activated by 3αDOG indicating different modes of activation by the two ligands. We show that an N-terminal truncated GPR56 construct (GPR56-Δ1-385) is devoid of constitutive activity but was activated by 3αDOG. Similarly to 3αDOG, 10C7 promoted the recruitment of β-arrestin-2 but GPR56 internalization was β-arrestin independent. Despite the slow activation mode of 10C7 that favors G13 over G12, it efficiently activated the downstream Rho pathway in BT-20 breast cancer cells. These data show that different GPR56 ligands have different modes of activation yielding differential G protein selectivity but converging on the activation of the Rho pathway both in heterologous expressions system and in cancer cells endogenously expressing the receptor. 10C7 is therefore an interesting tool to study both the processes underlying GPR56 activity and its role in cancer cells.","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"81 1","pages":"383"},"PeriodicalIF":6.2,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11374949/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142131987","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Lysosomal dysfunction in α-synuclein pathology: molecular mechanisms and therapeutic strategies. α-突触核蛋白病理学中的溶酶体功能障碍：分子机制和治疗策略。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2024-09-03 DOI: 10.1007/s00018-024-05419-5

Lijun Dai, Miao Liu, Wei Ke, Liam Chen, Xin Fang, Zhentao Zhang

{"title":"Lysosomal dysfunction in α-synuclein pathology: molecular mechanisms and therapeutic strategies.","authors":"Lijun Dai, Miao Liu, Wei Ke, Liam Chen, Xin Fang, Zhentao Zhang","doi":"10.1007/s00018-024-05419-5","DOIUrl":"10.1007/s00018-024-05419-5","url":null,"abstract":"In orchestrating cell signaling, facilitating plasma membrane repair, supervising protein secretion, managing waste elimination, and regulating energy consumption, lysosomes are indispensable guardians that play a crucial role in preserving intracellular homeostasis. Neurons are terminally differentiated post-mitotic cells. Neuronal function and waste elimination depend on normal lysosomal function. Converging data suggest that lysosomal dysfunction is a critical event in the etiology of Parkinson's disease (PD). Mutations in Glucosylceramidase Beta 1 (GBA1) and leucine-rich repeat kinase 2 (LRRK2) confer an increased risk for the development of parkinsonism. Furthermore, lysosomal dysfunction has been observed in the affected neurons of sporadic PD (sPD) patients. Given that lysosomal hydrolases actively contribute to the breakdown of impaired organelles and misfolded proteins, any compromise in lysosomal integrity could incite abnormal accumulation of proteins, including α-synuclein, the major component of Lewy bodies in PD. Clinical observations have shown that lysosomal protein levels in cerebrospinal fluid may serve as potential biomarkers for PD diagnosis and as signs of lysosomal dysfunction. In this review, we summarize the current evidence regarding lysosomal dysfunction in PD and discuss the intimate relationship between lysosomal dysfunction and pathological α-synuclein. In addition, we discuss therapeutic strategies that target lysosomes to treat PD.","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"81 1","pages":"382"},"PeriodicalIF":6.2,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11368888/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142119124","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The functions and mechanisms of piRNAs in mediating mammalian spermatogenesis and their applications in reproductive medicine. piRNA 介导哺乳动物精子发生的功能和机制及其在生殖医学中的应用。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2024-09-02 DOI: 10.1007/s00018-024-05399-6

Li Du, Wei Chen, Dong Zhang, Yinghong Cui, Zuping He

{"title":"The functions and mechanisms of piRNAs in mediating mammalian spermatogenesis and their applications in reproductive medicine.","authors":"Li Du, Wei Chen, Dong Zhang, Yinghong Cui, Zuping He","doi":"10.1007/s00018-024-05399-6","DOIUrl":"10.1007/s00018-024-05399-6","url":null,"abstract":"As the most abundant small RNAs, piwi-interacting RNAs (piRNAs) have been identified as a new class of non-coding RNAs with 24-32 nucleotides in length, and they are expressed at high levels in male germ cells. PiRNAs have been implicated in the regulation of several biological processes, including cell differentiation, development, and male reproduction. In this review, we focused on the functions and molecular mechanisms of piRNAs in controlling spermatogenesis, including genome stability, regulation of gene expression, and male germ cell development. The piRNA pathways include two major pathways, namely the pre-pachytene piRNA pathway and the pachytene piRNA pathway. In the pre-pachytene stage, piRNAs are involved in chromosome remodeling and gene expression regulation to maintain genome stability by inhibiting transposon activity. In the pachytene stage, piRNAs mediate the development of male germ cells via regulating gene expression by binding to mRNA and RNA cleavage. We further discussed the correlations between the abnormalities of piRNAs and male infertility and the prospective of piRNAs' applications in reproductive medicine and future studies. This review provides novel insights into mechanisms underlying mammalian spermatogenesis and offers new targets for diagnosing and treating male infertility.","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"81 1","pages":"379"},"PeriodicalIF":6.2,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11369131/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142104839","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0