Progress in Molecular Biology and Translational Science最新文献_第4页

COVID-19: Perspectives on innate immune evasion. COVID-19：对先天免疫逃避的看法。

3区生物学

Progress in Molecular Biology and Translational Science Pub Date : 2025-01-01 Epub Date: 2024-03-19 DOI: 10.1016/bs.pmbts.2024.03.002

Alaa A A Aljabali, Mohamed El-Tanani, Debmalya Barh, Murtaza M Tambuwala

{"title":"COVID-19: Perspectives on innate immune evasion.","authors":"Alaa A A Aljabali, Mohamed El-Tanani, Debmalya Barh, Murtaza M Tambuwala","doi":"10.1016/bs.pmbts.2024.03.002","DOIUrl":"https://doi.org/10.1016/bs.pmbts.2024.03.002","url":null,"abstract":"The ongoing global health challenges posed by the SARS-CoV-2, the virus responsible for the COVID-19 pandemic, necessitate a deep understanding of its intricate strategies to evade the innate immune system. This chapter aims to provide insights into the sophisticated mechanisms employed by SARS-CoV-2 in its interaction with pattern recognition receptors (PRRs), with particular emphasis on Toll-like receptors (TLRs) and RIG-I-like receptors (RLRs). By skillfully circumventing these pivotal components, the virus manages to elude detection and impairs the initiation of crucial antiviral immune responses. A notable aspect of SARS-CoV-2's immune evasion tactics lies in its strategic manipulation of cytokine production. This orchestrated modulation disrupts the delicate balance of inflammation, potentially leading to severe complications, including the notorious cytokine storm. In this regard, key viral proteins, such as the spike protein and nucleocapsid protein, emerge as pivotal players in the immune evasion process, further highlighting their significance in the context of COVID-19 pathogenesis. Acquiring a comprehensive understanding of these intricate immune evasion mechanisms holds immense promise for the development of effective treatments against COVID-19. Moreover, it is imperative for vaccine development to consider these evasion strategies to maximize vaccine efficacy. Future therapeutic interventions may involve targeting alternative pathways or augmenting the antiviral immune responses, thereby mitigating the impact of immune evasion, and fostering successful outcomes. By unraveling the underlying mechanisms of innate immune evasion, we advance our comprehension of COVID-19 pathogenesis and pave the way for the development of innovative therapeutic strategies. This comprehensive understanding catalyzes progress, enabling researchers and clinicians to devise novel approaches that combat the challenges posed by SARS-CoV-2 and ultimately improve patient outcomes.","PeriodicalId":49280,"journal":{"name":"Progress in Molecular Biology and Translational Science","volume":"213 ","pages":"171-214"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144028139","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Impact of COVID-19 on preexisting comorbidities. COVID-19对先前存在的合并症的影响。

3区生物学

Progress in Molecular Biology and Translational Science Pub Date : 2025-01-01 Epub Date: 2025-01-31 DOI: 10.1016/bs.pmbts.2024.10.002

Rasha Ashmawy, Esraa Abdellatif Hamouda, Sally Zeina, Sandy Sharaf, Sara Erfan, Elrashdy M Redwan

引用次数: 0

The Huntington's disease drug pipeline: a review of small molecules and their therapeutic targets. 亨廷顿氏病药物管道：小分子及其治疗靶点综述。

3区生物学

Progress in Molecular Biology and Translational Science Pub Date : 2025-01-01 Epub Date: 2024-10-16 DOI: 10.1016/bs.pmbts.2024.08.006

Sameera Khan, Nargis Bano, Vladimir N Uversky, Shakir Ahamad, Shahnawaz Ali Bhat

{"title":"The Huntington's disease drug pipeline: a review of small molecules and their therapeutic targets.","authors":"Sameera Khan, Nargis Bano, Vladimir N Uversky, Shakir Ahamad, Shahnawaz Ali Bhat","doi":"10.1016/bs.pmbts.2024.08.006","DOIUrl":"10.1016/bs.pmbts.2024.08.006","url":null,"abstract":"Huntington's disease (HD) is a progressive neurodegenerative condition resulting from a CAG repeat expansion in the huntingtin gene (HTT). Recent advancements in understanding HD's cellular and molecular pathways have paved the way for identifying various effective small-molecule candidates to treat the disorder. Two small molecules, Tetrabenazine and Deutetrabenazine, are approved for managing chorea associated with HD, and several others are under clinical trials. Notably, the field of small-molecule therapeutics targeting HD is rapidly progressing, and there is anticipation of their approval in the foreseeable future. This chapter provides a comprehensive overview of the emergence of small-molecule therapeutics in various stages of clinical development for HD therapy. The emphasis is placed on detailing their structural design, therapeutic effects, and specific mechanisms of action. Additionally, exploring key drivers implicated in HD pathogenesis offers valuable insights, as a foundational principle for designing prospective anti-HD therapeutic leads.","PeriodicalId":49280,"journal":{"name":"Progress in Molecular Biology and Translational Science","volume":"211 ","pages":"169-207"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143415908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Strategies for inhibiting amyloid fibrillation: Current status and future prospects. 抑制淀粉样蛋白颤动的策略：现状和未来展望。

3区生物学

Progress in Molecular Biology and Translational Science Pub Date : 2025-01-01 Epub Date: 2025-01-21 DOI: 10.1016/bs.pmbts.2024.09.001

Md Nadir Hassan, Murtaza Hussain, Rizwan Hasan Khan

引用次数: 0

Preface. 前言。

3区生物学

Progress in Molecular Biology and Translational Science Pub Date : 2025-01-01 DOI: 10.1016/S1877-1173(25)00177-2

Vijay Kumar Prajapati

引用次数: 0

The impact of COVID-19 on autoimmune diseases. COVID-19对自身免疫性疾病的影响。

3区生物学

Progress in Molecular Biology and Translational Science Pub Date : 2025-01-01 Epub Date: 2025-02-25 DOI: 10.1016/bs.pmbts.2025.01.007

Altijana Hromić-Jahjefendić, Abas Sezer, Irma Mahmuljin

{"title":"The impact of COVID-19 on autoimmune diseases.","authors":"Altijana Hromić-Jahjefendić, Abas Sezer, Irma Mahmuljin","doi":"10.1016/bs.pmbts.2025.01.007","DOIUrl":"https://doi.org/10.1016/bs.pmbts.2025.01.007","url":null,"abstract":"Various autoantibodies, such as antinuclear antibodies (ANA), anti-Ro/SSA, rheumatoid factor, lupus anticoagulant, and antibodies against interferon type I (IFN-I), have been frequently detected in COVID-19 patients, indicating a significant prevalence of autoimmune reactions following viral exposure. Additionally, the identification of human proteins with structural similarities to SARS-CoV-2 peptides as potential autoantigens underscores the complex interplay between the virus and the immune system in triggering autoimmunity. The chapter discusses probable pathways contributing to COVID-19-related autoimmunity, including bystander activation due to hyperinflammatory states, viral persistence, and the formation of neutrophil extracellular traps. These mechanisms illuminate a spectrum of autoimmune-related symptoms that can manifest, ranging from organ-specific to systemic autoimmune and inflammatory diseases. Importantly, there is emerging evidence of de novo autoimmunity arising after COVID-19 infection or vaccination, where new autoimmune conditions develop in previously healthy individuals. While various COVID-19 vaccines have received emergency use authorization, concerns regarding potential autoimmune side effects persist. Ongoing research is crucial to clarify these relationships and enhance our understanding of the risks associated with COVID-19 infections and vaccinations.","PeriodicalId":49280,"journal":{"name":"Progress in Molecular Biology and Translational Science","volume":"213 ","pages":"315-345"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144043953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Factors responsible for alpha-Synuclein aggregation. 负责α -突触核蛋白聚集的因子。

3区生物学

Progress in Molecular Biology and Translational Science Pub Date : 2025-01-01 Epub Date: 2025-01-25 DOI: 10.1016/bs.pmbts.2024.11.004

Khuraijam Surjalal Singh, Rahul Verma, Nagendra Singh, Laishram Rajendrakumar Singh, Akshita Gupta

{"title":"Factors responsible for alpha-Synuclein aggregation.","authors":"Khuraijam Surjalal Singh, Rahul Verma, Nagendra Singh, Laishram Rajendrakumar Singh, Akshita Gupta","doi":"10.1016/bs.pmbts.2024.11.004","DOIUrl":"10.1016/bs.pmbts.2024.11.004","url":null,"abstract":"Aggregation of α-Synuclein (α-Syn) is the hallmark of the pathophysiology of Parkinson's disease. Apart from aggregates, α-Syn can exist in multiple abnormal forms such as oligomers, protofibrils, fibrils amorphous aggregates etc. These forms initiate aggressive, selective and progressive neuronal atrophy through various modes such as mitochondrial dysfunction, lysosomal malfunction, and disruption of calcium homeostasis in various α-Syn-related neurodegenerative disorders. Structurally α-Syn is divided into three domains: N-terminal region made by amino acids1-67 (amphipathic, lysine-rich and interacts with acidic lipid membranes), Non-amyloid-β component (NAC) region made by amino acids 67-95 (hydrophobic region, central to α-syn aggregation) and C-terminal region made by amino acids 96-140 (acidic and proline-rich region responsible for interaction with other proteins). α-Syn follows the pattern of a typical intrinsically disordered protein and lacks a proper folded conformation and exist majorly in a random coil form, though on lipid binding the protein assumes an α-helical structure. The central random coil region of α-Syn is involved in fibril formation transforming into β-sheet rich secondary structures which is a characteristic of amyloids. This chapter entails an elaborate explanation of factors influencing the structure, function and aggregation of α-Syn. Major factors being abnormally high physiological expression of the protein, mutations, posttranslational modifications and also interactions with small molecules such as osmolytes in the cellular milieu. Studying the factors responsible for misfolding and aggregation of α-Syn along with the mechanism involved is crucial to understanding their implications in Parkinson's disease, and will yield valuable insights into disease mechanisms, potential therapeutic strategies.","PeriodicalId":49280,"journal":{"name":"Progress in Molecular Biology and Translational Science","volume":"211 ","pages":"271-292"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143415501","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Cell death triad: Integrating apoptotic, autophagic, and necrotic cell death mechanisms. 细胞死亡三位一体：整合凋亡、自噬和坏死细胞死亡机制。

3区生物学

Progress in Molecular Biology and Translational Science Pub Date : 2025-01-01 Epub Date: 2025-07-01 DOI: 10.1016/bs.pmbts.2025.06.017

Sarthak Dhar, Kirti Baghel, Sramona Kar, Sanjana Mehrotra, Vijay Kumar Prajapati

{"title":"Cell death triad: Integrating apoptotic, autophagic, and necrotic cell death mechanisms.","authors":"Sarthak Dhar, Kirti Baghel, Sramona Kar, Sanjana Mehrotra, Vijay Kumar Prajapati","doi":"10.1016/bs.pmbts.2025.06.017","DOIUrl":"https://doi.org/10.1016/bs.pmbts.2025.06.017","url":null,"abstract":"Cell death mechanisms represent fundamental biological processes essential for homeostasis, development, and disease response. Recent advances have expanded our comprehension of these processes and contributed to the identification of novel mechanisms that orchestrate these processes. Apoptosis, a well-characterized form of cell death involving characteristic morphological changes and multiple enzymes that orchestrate the biochemical process, with minimal damage to surrounding cells or tissues and clearing off the apoptotic bodies by phagocytic cells. Dysregulation in the biochemical process could eventually lead to various pathologies including cancer and neurodegenerative disorders. Autophagy primarily a cell survival process that recycles cellular components, can paradoxically contribute to cell death under specific conditions especially when apoptosis is inhibited. Necrosis, once considered purely accidental, is now recognized to include regulated forms such as necroptosis, with defined molecular triggers and execution pathways. In this review, we will explore a general overview of the current comprehension of these major known cell death pathways such as apoptosis, autophagic cell death, necrosis, and necroptosis along with their crosstalk and potential targets in the biochemical mechanisms for therapeutic modulation of these processes that have major clinical implications.","PeriodicalId":49280,"journal":{"name":"Progress in Molecular Biology and Translational Science","volume":"217 ","pages":"1-23"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145126268","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Role and relation of cell death in Alzheimer's disease. 细胞死亡在阿尔茨海默病中的作用和关系。

3区生物学

Progress in Molecular Biology and Translational Science Pub Date : 2025-01-01 Epub Date: 2025-07-01 DOI: 10.1016/bs.pmbts.2025.06.024

Duc Anh Hoang, Duc Anh Le, Thi My Hanh Do, Van Thai Than

引用次数: 0

Cell death mechanisms in Drosophila: Responses to infectious challenges. 果蝇的细胞死亡机制：对感染挑战的反应。

3区生物学

Progress in Molecular Biology and Translational Science Pub Date : 2025-01-01 Epub Date: 2025-07-31 DOI: 10.1016/bs.pmbts.2025.07.002

Gaurav Yadav, Shrishti Mitra, Raunak Gupta, Prachi Mishra, Dau Dayal Aggarwal

{"title":"Cell death mechanisms in Drosophila: Responses to infectious challenges.","authors":"Gaurav Yadav, Shrishti Mitra, Raunak Gupta, Prachi Mishra, Dau Dayal Aggarwal","doi":"10.1016/bs.pmbts.2025.07.002","DOIUrl":"https://doi.org/10.1016/bs.pmbts.2025.07.002","url":null,"abstract":"Cell death, a highly conserved and regulated process, plays a key role in development of an organism, immune responses, and tissue homeostasis. Often viewed in a negative light, it tightly regulates the proper balance of cell numbers and this fine balance carries the weight of life. In Drosophila melanogaster, a well-established genetic model, several forms of cell death including autophagy, apoptosis, and necrosis-like pathways are observed in response to the diverse bodily signals and infections. These distinct cell deaths are triggered through specific signaling pathways such as the Jun N-terminal kinase (JNK) pathway, the Toll and Imd immune pathways, and mitochondrial reactive oxygen species (ROS) mediated responses. This chapter explores the molecular regulation of these cell death pathways, emphasizing tissue-specific responses in Drosophila during bacterial and fungal infections. By understanding how various tissues, including the brain, gut, fat body, and muscles, differentially regulate cell death, we gain valuable insights into evolutionarily conserved strategies for host defense. Understanding these mechanisms helps reveal key biological principles relevant to immunity, pathology, and therapeutic development.","PeriodicalId":49280,"journal":{"name":"Progress in Molecular Biology and Translational Science","volume":"217 ","pages":"233-262"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145126303","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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