Cell insightPub Date : 2025-04-11DOI: 10.1016/j.cellin.2025.100239
Xiaoyu Song , Yufeng Xi , Ming Dai , Tao Li , Shihao Du , Yuxin Zhu , Mengjie Li , Yunze Li , Siqi Liu , Xia Ding , Xuebiao Yao , Ying Lai , Xing Liu
{"title":"Corrigendum to “STING guides the STX17-SNAP29-VAMP8 complex assembly to control autophagy” [Cell Insight 3 (2024) 100147]","authors":"Xiaoyu Song , Yufeng Xi , Ming Dai , Tao Li , Shihao Du , Yuxin Zhu , Mengjie Li , Yunze Li , Siqi Liu , Xia Ding , Xuebiao Yao , Ying Lai , Xing Liu","doi":"10.1016/j.cellin.2025.100239","DOIUrl":"10.1016/j.cellin.2025.100239","url":null,"abstract":"","PeriodicalId":72541,"journal":{"name":"Cell insight","volume":"4 3","pages":"Article 100239"},"PeriodicalIF":0.0,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143815801","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell insightPub Date : 2025-03-31DOI: 10.1016/j.cellin.2025.100240
Meimei Guo , Feiyang Zhang , Sha Liu , Yi Zhang , Lesheng Wang , Jian Song , Wei Wei , Xiang Li
{"title":"The role of TRPV4 in acute sleep deprivation-induced memory impairment: Mechanisms of calcium dysregulation and synaptic plasticity disruption","authors":"Meimei Guo , Feiyang Zhang , Sha Liu , Yi Zhang , Lesheng Wang , Jian Song , Wei Wei , Xiang Li","doi":"10.1016/j.cellin.2025.100240","DOIUrl":"10.1016/j.cellin.2025.100240","url":null,"abstract":"<div><div>Acute sleep deprivation (ASD) impairs memory formation, but the underlying mechanisms remain unclear. In this study, we employed an ASD model combined with fear conditioning to investigate these mechanisms. mRNA sequencing revealed upregulated expression of Transient Receptor Potential Vanilloid 4 (TRPV4), a nonselective Ca<sup>2+</sup>-permeable cation channel critical for calcium signaling, in mice with ASD-induced memory impairments. Notably, TRPV4 knockdown reversed ASD-induced memory deficits. ASD was associated with increased intracellular Ca<sup>2+</sup> concentrations, reduced spine density, and decreased expression of postsynaptic density protein 95 (PSD95), a key regulator of synaptic plasticity. These findings suggest that ASD may cause Ca<sup>2+</sup> overload, leading to disrupted synaptic plasticity and impaired learning and memory. Importantly, TRPV4 knockdown significantly reduced Ca<sup>2+</sup> concentrations, mitigated synaptic plasticity impairments, and contributed to memory restoration. Together, these findings demonstrate a protective role of TRPV4 knockdown against ASD-induced memory deficits and highlight TRPV4 as a potential therapeutic target for memory impairment associated with ASD.</div></div>","PeriodicalId":72541,"journal":{"name":"Cell insight","volume":"4 3","pages":"Article 100240"},"PeriodicalIF":0.0,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143815800","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell insightPub Date : 2025-02-17DOI: 10.1016/j.cellin.2025.100238
Abdalla Elbialy , Akshay Sood , Shang-Jui Wang , Peng Wang , Ahmed Fadiel , Anil V. Parwani , Steven Huang , Gennady Shvets , Nagireddy Putluri , Jenny Li , Xuefeng Liu
{"title":"Unveiling racial disparities in prostate cancer using an integrative genomic and transcriptomic analysis","authors":"Abdalla Elbialy , Akshay Sood , Shang-Jui Wang , Peng Wang , Ahmed Fadiel , Anil V. Parwani , Steven Huang , Gennady Shvets , Nagireddy Putluri , Jenny Li , Xuefeng Liu","doi":"10.1016/j.cellin.2025.100238","DOIUrl":"10.1016/j.cellin.2025.100238","url":null,"abstract":"<div><div>Prostate cancer exhibits significant racial disparities, with African American (AA) individuals showing ∼64% higher incidence and 2.3 times greater mortality rates compared to their Caucasian (CA) counterparts. Understanding the complex interplay of genetic, environmental, lifestyle, socioeconomic, and healthcare access factors is crucial for developing effective interventions to reduce this disproportionate burden.</div><div>This study aims to uncover the genetic and transcriptomic differences driving these disparities through a comprehensive analysis using RNA sequencing (RNA-seq) and exome sequencing of prostate cancer tissues from both Black and White patients.</div><div>Our transcriptomics analysis revealed enhanced activity in pathways linked to immune response and cellular interactions in AA prostate cancer samples, with notable regulation by histone-associated transcription factors (HIST1H1A, HIST1H1D, and HIST1H1B) suggests potential involvement of histone modification mechanisms. Additionally, pseudogenes and long non-coding RNAs (lncRNAs) among the regulated genes indicate non-coding elements' role in these disparities.</div><div>Exome sequencing identified unique variants in AA patient samples within key genes, including TP73 (tumor suppression), XYLB (metabolism), ALDH4A1 (oxidative stress), PTPRB (cellular signaling), and HLA-DRB5 (immune response). These genetic variations likely contribute to disease progression and therapy response disparities.</div><div>This study highlights the importance of considering genetic and epigenetic variations in developing tailored therapeutic approaches to improve treatment efficacy and reduce mortality rates across diverse populations.</div></div>","PeriodicalId":72541,"journal":{"name":"Cell insight","volume":"4 2","pages":"Article 100238"},"PeriodicalIF":0.0,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143511092","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell insightPub Date : 2025-02-13DOI: 10.1016/j.cellin.2025.100237
Hongyu Zhao , Xinyue Zhang , Ningning Zhang , Li Zhu , Huan Lian
{"title":"The interplay between Salmonella and host: Mechanisms and strategies for bacterial survival","authors":"Hongyu Zhao , Xinyue Zhang , Ningning Zhang , Li Zhu , Huan Lian","doi":"10.1016/j.cellin.2025.100237","DOIUrl":"10.1016/j.cellin.2025.100237","url":null,"abstract":"<div><div>Salmonella, an intracellular pathogen, infects both humans and animals, causing diverse diseases such as gastroenteritis and enteric fever. The <em>Salmonella</em> type III secretion system (T3SS), encoded within its pathogenicity islands (SPIs), is critical for bacterial virulence by directly delivering multiple effectors into eukaryotic host cells. <em>Salmonella</em> utilizes these effectors to facilitate its survival and replication within the host through modulating cytoskeletal dynamics, inflammatory responses, the biogenesis of <em>Salmonella</em>-containing vacuole (SCV), and host cell survival. Moreover, these effectors also interfere with immune responses via inhibiting innate immunity or antigen presentation. In this review, we summarize the current progress in the survival strategies employed by <em>Salmonella</em> and the molecular mechanisms underlying its interactions with the host. Understanding the interplay between <em>Salmonella</em> and host can enhance our knowledge of the bacterium's pathogenic processes and provide new insights into how it manipulates host cellular physiological activities to ensure its survival.</div></div>","PeriodicalId":72541,"journal":{"name":"Cell insight","volume":"4 2","pages":"Article 100237"},"PeriodicalIF":0.0,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143643372","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell insightPub Date : 2025-02-01DOI: 10.1016/j.cellin.2024.100224
Chao Chen , Xinjian Li
{"title":"The cell autonomous and non-autonomous roles of itaconate in immune response","authors":"Chao Chen , Xinjian Li","doi":"10.1016/j.cellin.2024.100224","DOIUrl":"10.1016/j.cellin.2024.100224","url":null,"abstract":"<div><div>Itaconate which is discovered as a mammalian metabolite possessing antimicrobial and immunoregulatory activity has attracted much attention in the field of immunometabolism. Itaconate is synthesized by myeloid cells under conditions of pathogen infection and sterile inflammation. In addition to regulating immune response of myeloid cells, itaconate secreted from myeloid cells can also be taken up by non-myeloid cells to exert immunoregulatory effects in a cell non-autonomous manner. In this review, we recap the discovery of itaconate as a distinct immunologic regulator and effector, describe the development of itaconate biosensor, and detail the recent findings that decipher the mechanism underlying intercellular transport of itaconate. Based on these knowledges, we propose itaconate is a messenger transmitting immunologic signals from myeloid cells to other types of cells during host inflammation and immune defense.</div></div>","PeriodicalId":72541,"journal":{"name":"Cell insight","volume":"4 1","pages":"Article 100224"},"PeriodicalIF":0.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11773213/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143061127","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell insightPub Date : 2025-02-01DOI: 10.1016/j.cellin.2024.100223
Yuxin Du , Yin Shen
{"title":"Progress in photoreceptor replacement therapy for retinal degenerative diseases","authors":"Yuxin Du , Yin Shen","doi":"10.1016/j.cellin.2024.100223","DOIUrl":"10.1016/j.cellin.2024.100223","url":null,"abstract":"<div><div>Retinal degenerative diseases encompass a diverse range of eye conditions that result in blindness, many due to photoreceptor dysfunction and loss. Regrettably, current clinical treatments are frequently not overly effective. However, photoreceptor transplantation shows promise as a potential therapy for late-stage retinal degenerative diseases. This article will review the various donor cell sources for this transplantation, as well as the mechanisms and factors that impact donor cell integration and material transfer, donor cell maturation, and other auxiliary methods that can be combined with photoreceptor transplantation to treat these degenerative retinal diseases.</div></div>","PeriodicalId":72541,"journal":{"name":"Cell insight","volume":"4 1","pages":"Article 100223"},"PeriodicalIF":0.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11773227/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143061184","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell insightPub Date : 2025-01-20DOI: 10.1016/j.cellin.2025.100228
Xiaohan Tong , Tianle Li , Kun Zhang , Dongming Zhao , Ying Zhang , Hao Yin
{"title":"Structure-Guided design of Cas12a variants improves detection of nucleic acids","authors":"Xiaohan Tong , Tianle Li , Kun Zhang , Dongming Zhao , Ying Zhang , Hao Yin","doi":"10.1016/j.cellin.2025.100228","DOIUrl":"10.1016/j.cellin.2025.100228","url":null,"abstract":"<div><div>CRISPR-Cas12a holds promising potential for pathogen detection. However, its performance is not optimal when combined with isothermal amplification. Hence, we engineered a mutant of LbCas12a (K595A) with reduced <em>cis</em>-cleavage activity, to minimize interference with isothermal amplification. Compared to wild-type Cas12a, the K595A mutant exhibited a 2–3 times faster reaction speed and a 1,000–10,000 times increase in sensitivity in a one-pot reaction. We applied this mutant for detection of African Swine Fever Virus (ASFV). This K595A mutant successfully detected all 30 ASFV samples within 20 minutes. Our study suggests a universal approach to improve the performance of Cas12a for pathogen detection.</div></div>","PeriodicalId":72541,"journal":{"name":"Cell insight","volume":"4 2","pages":"Article 100228"},"PeriodicalIF":0.0,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143445939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell insightPub Date : 2025-01-18DOI: 10.1016/j.cellin.2025.100229
Xinming Su , Qingyuan Lin , Bin Liu , Chuntao Zhou , Liuyi Lu , Zihao Lin , Jiahua Si , Yuemin Ding , Shiwei Duan
{"title":"The promising role of nanopore sequencing in cancer diagnostics and treatment","authors":"Xinming Su , Qingyuan Lin , Bin Liu , Chuntao Zhou , Liuyi Lu , Zihao Lin , Jiahua Si , Yuemin Ding , Shiwei Duan","doi":"10.1016/j.cellin.2025.100229","DOIUrl":"10.1016/j.cellin.2025.100229","url":null,"abstract":"<div><div>Cancer arises from genetic alterations that impact both the genome and transcriptome. The utilization of nanopore sequencing offers a powerful means of detecting these alterations due to its unique capacity for long single-molecule sequencing. In the context of DNA analysis, nanopore sequencing excels in identifying structural variations (SVs), copy number variations (CNVs), gene fusions within SVs, and mutations in specific genes, including those involving DNA modifications and DNA adducts. In the field of RNA research, nanopore sequencing proves invaluable in discerning differentially expressed transcripts, uncovering novel elements linked to transcriptional regulation, and identifying alternative splicing events and RNA modifications at the single-molecule level. Furthermore, nanopore sequencing extends its reach to detecting microorganisms, encompassing bacteria and viruses, that are intricately associated with tumorigenesis and the development of cancer. Consequently, the application prospects of nanopore sequencing in tumor diagnosis and personalized treatment are expansive, encompassing tasks such as tumor identification and classification, the tailoring of treatment strategies, and the screening of prospective patients. In essence, this technology stands poised to unearth novel mechanisms underlying tumorigenesis while providing dependable support for the diagnosis and treatment of cancer.</div></div>","PeriodicalId":72541,"journal":{"name":"Cell insight","volume":"4 2","pages":"Article 100229"},"PeriodicalIF":0.0,"publicationDate":"2025-01-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143265220","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}