Pub Date : 2025-10-15DOI: 10.1016/j.pbiomolbio.2025.10.002
Xinzheng Wang , Huifen Zhou
Ischemic stroke (IS) is a leading cause of disability and mortality worldwide, with mitochondrial dysfunction being a fundamental pathological mechanism. This dysfunction involves a dynamic imbalance, diminished biosynthesis, oxidative stress, and dysregulated autophagy. Exercise, a promising non-pharmacological intervention, can ameliorate this dysfunction, but its precise molecular mechanisms remain to be fully elucidated. This review synthesizes evidence demonstrating that exercise enhances mitochondrial morphology and function through various pathways, including the promotion of mitochondrial biogenesis, the regulation of mitochondrial ROS, and the modulation of mitochondrial dynamics and mitophagy, thereby mitigating functional impairments associated with IS. Critically, the beneficial effects of exercise are dose dependent, highlighting the necessity for personalized exercise prescriptions on the basis of individual patient profiles. Elucidating these mechanisms provides a crucial theoretical foundation for developing exercise-based strategies for the prevention and treatment of IS.
{"title":"Exercise as a therapeutic strategy against mitochondrial dysfunction in ischemic stroke: Molecular mechanisms and perspectives for personalized treatment","authors":"Xinzheng Wang , Huifen Zhou","doi":"10.1016/j.pbiomolbio.2025.10.002","DOIUrl":"10.1016/j.pbiomolbio.2025.10.002","url":null,"abstract":"<div><div>Ischemic stroke (IS) is a leading cause of disability and mortality worldwide, with mitochondrial dysfunction being a fundamental pathological mechanism. This dysfunction involves a dynamic imbalance, diminished biosynthesis, oxidative stress, and dysregulated autophagy. Exercise, a promising non-pharmacological intervention, can ameliorate this dysfunction, but its precise molecular mechanisms remain to be fully elucidated. This review synthesizes evidence demonstrating that exercise enhances mitochondrial morphology and function through various pathways, including the promotion of mitochondrial biogenesis, the regulation of mitochondrial ROS, and the modulation of mitochondrial dynamics and mitophagy, thereby mitigating functional impairments associated with IS. Critically, the beneficial effects of exercise are dose dependent, highlighting the necessity for personalized exercise prescriptions on the basis of individual patient profiles. Elucidating these mechanisms provides a crucial theoretical foundation for developing exercise-based strategies for the prevention and treatment of IS.</div></div>","PeriodicalId":54554,"journal":{"name":"Progress in Biophysics & Molecular Biology","volume":"198 ","pages":"Pages 55-60"},"PeriodicalIF":4.5,"publicationDate":"2025-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145314128","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}
Pub Date : 2025-10-01DOI: 10.1016/j.pbiomolbio.2025.10.001
Asrin Emami , Iman Menbari Oskouie
Bone regeneration remains one of the greatest challenges in orthopedic medicine, particularly in cases of complex fractures, nonhealing bones, or large bone defects. Traditional treatments, such as autologous grafts, allogeneic grafts, synthetic materials, or drug therapies, often face limitations, including donor-site pain, immune rejection, and limited ability to stimulate true bone healing. A promising new approach involves the use of exosome-enhanced scaffolds, which combine the structural support of biomaterial scaffolds with the potent regenerative effects of exosomes. Exosomes are nanosized vesicles secreted by cells such as mesenchymal stem cells, osteoblasts, and macrophages. They carry proteins, lipids, and regulatory RNAs that play crucial roles in coordinating bone formation, angiogenesis, and immune modulation. When incorporated into scaffolds, exosomes promote osteogenesis, stimulate vascularization, and facilitate tissue remodeling, thereby creating an optimal microenvironment for bone repair. Preclinical studies have demonstrated accelerated healing, enhanced bone strength, and improved overall bone quality, while early clinical trials indicate that these therapies are both safe and effective. Current research efforts focus on optimizing exosome isolation, understanding their interactions with scaffolds, and developing controlled delivery systems. This strategy holds great promise for transforming orthopedic care by providing patient-specific, biologically active treatments for even the most challenging bone defects.
{"title":"From bench to Bone: Clinical promise of exosome-enhanced scaffolds in orthopedic regeneration","authors":"Asrin Emami , Iman Menbari Oskouie","doi":"10.1016/j.pbiomolbio.2025.10.001","DOIUrl":"10.1016/j.pbiomolbio.2025.10.001","url":null,"abstract":"<div><div>Bone regeneration remains one of the greatest challenges in orthopedic medicine, particularly in cases of complex fractures, nonhealing bones, or large bone defects. Traditional treatments, such as autologous grafts, allogeneic grafts, synthetic materials, or drug therapies, often face limitations, including donor-site pain, immune rejection, and limited ability to stimulate true bone healing. A promising new approach involves the use of exosome-enhanced scaffolds, which combine the structural support of biomaterial scaffolds with the potent regenerative effects of exosomes. Exosomes are nanosized vesicles secreted by cells such as mesenchymal stem cells, osteoblasts, and macrophages. They carry proteins, lipids, and regulatory RNAs that play crucial roles in coordinating bone formation, angiogenesis, and immune modulation. When incorporated into scaffolds, exosomes promote osteogenesis, stimulate vascularization, and facilitate tissue remodeling, thereby creating an optimal microenvironment for bone repair. Preclinical studies have demonstrated accelerated healing, enhanced bone strength, and improved overall bone quality, while early clinical trials indicate that these therapies are both safe and effective. Current research efforts focus on optimizing exosome isolation, understanding their interactions with scaffolds, and developing controlled delivery systems. This strategy holds great promise for transforming orthopedic care by providing patient-specific, biologically active treatments for even the most challenging bone defects.</div></div>","PeriodicalId":54554,"journal":{"name":"Progress in Biophysics & Molecular Biology","volume":"198 ","pages":"Pages 32-38"},"PeriodicalIF":4.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145219857","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}
Nanoparticles and viruses share several similarities and link the fields of physical and biological sciences by covering and overlapping both realms. In this review we have discussed their commonalities based on classification of constituent material, mode of replication and origin, size, as well as function and application in cargo delivery. We have discussed the modulatory and characteristics of each subunit and how it contributes to cellular uptake and replication. We have also gone into their environmental roles in nutrient mobilization and cycling, being subject to and themselves exerting evolutionary pressures as well as their final environmental fates of immobilization and disintegration. Finally, we have explored their potential use in environmental remediation and energy generation. The novelty of this work is in signifying that both nanoparticles and viruses fall into the realm of macro-biomolecular or nano assemblies and are in many ways similar in origin, characteristics and can be often used synergistically to solve contemporary problems.
{"title":"Exploring the parallels between nanoparticles and viruses with emphasis on environmental roles and remediation","authors":"Mahima Kaushik , Madhu Pruthi , Arpana Sharma , Radhey Shyam Sharma , Vandana Mishra , Swagata Karmakar , Niloy Sarkar","doi":"10.1016/j.pbiomolbio.2025.09.003","DOIUrl":"10.1016/j.pbiomolbio.2025.09.003","url":null,"abstract":"<div><div>Nanoparticles and viruses share several similarities and link the fields of physical and biological sciences by covering and overlapping both realms. In this review we have discussed their commonalities based on classification of constituent material, mode of replication and origin, size, as well as function and application in cargo delivery. We have discussed the modulatory and characteristics of each subunit and how it contributes to cellular uptake and replication. We have also gone into their environmental roles in nutrient mobilization and cycling, being subject to and themselves exerting evolutionary pressures as well as their final environmental fates of immobilization and disintegration. Finally, we have explored their potential use in environmental remediation and energy generation. The novelty of this work is in signifying that both nanoparticles and viruses fall into the realm of macro-biomolecular or nano assemblies and are in many ways similar in origin, characteristics and can be often used synergistically to solve contemporary problems.</div></div>","PeriodicalId":54554,"journal":{"name":"Progress in Biophysics & Molecular Biology","volume":"198 ","pages":"Pages 39-54"},"PeriodicalIF":4.5,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145208465","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}
Pub Date : 2025-09-13DOI: 10.1016/j.pbiomolbio.2025.09.002
Sodikdjon A. Kodirov
The observation of non-linear current-voltage relationships of membrane potential responses in neurons led to the discovery of hyperpolarization-induced membrane conductance. The main underlying hallmark of this conductance was the presence of sag – spontaneous depolarization of membrane potential during constant hyperpolarization in current-clamp mode. Gradually, the presence of underling hyperpolarization-activated cyclic nucleotide-gated non-selective cation channels (HCN, Ih, or If, where f is for funny) was established. The earliest delineation of HCN-mediated sag in the hippocampus was documented by Purpura, Prelevic, and Santini with a short communication in 1968. The study was performed using classical electrophysiology by impaling the perikaryon of hippocampal neurons, but the outcomes are as insightful as with the patch-clamp technique, and the quality of traces exceeds some of the recent recordings. However, the latter authors were not convinced that the sag phenomenon could play a role under physiological conditions. It is logical since a depolarization and linked excitability are frequently observed in vivo, but not a hyperpolarization. At least a sudden, sharp hyperpolarization does not occur in the CNS. Besides, in order to activate the HCN channels, the amplitude and duration of hyperpolarization should be significant and sufficient. Nonetheless, those with skepticism conveyed pioneer observations were pivotal, since the presence of sag – activation of HCN channels – may also play a role in autism and epilepsy.
{"title":"Delineation and functions of HCN channels in neurons","authors":"Sodikdjon A. Kodirov","doi":"10.1016/j.pbiomolbio.2025.09.002","DOIUrl":"10.1016/j.pbiomolbio.2025.09.002","url":null,"abstract":"<div><div>The observation of non-linear current-voltage relationships of membrane potential responses in neurons led to the discovery of hyperpolarization-induced membrane conductance. The main underlying hallmark of this conductance was the presence of sag – spontaneous depolarization of membrane potential during constant hyperpolarization in current-clamp mode. Gradually, the presence of underling hyperpolarization-activated cyclic nucleotide-gated non-selective cation channels (HCN, <em>I</em><sub>h</sub>, or <em>I</em><sub>f</sub>, where <em>f</em> is for funny) was established. The earliest delineation of HCN-mediated sag in the hippocampus was documented by Purpura, Prelevic, and Santini with a short communication in 1968. The study was performed using classical electrophysiology by impaling the perikaryon of hippocampal neurons, but the outcomes are as insightful as with the patch-clamp technique, and the quality of traces exceeds some of the recent recordings. However, the latter authors were not convinced that the sag phenomenon could play a role under physiological conditions. It is logical since a depolarization and linked excitability are frequently observed in <em>vivo</em>, but not a hyperpolarization. At least a sudden, sharp hyperpolarization does not occur in the CNS. Besides, in order to activate the HCN channels, the amplitude and duration of hyperpolarization should be significant and sufficient. Nonetheless, those with skepticism conveyed pioneer observations were pivotal, since the presence of sag – activation of HCN channels – may also play a role in autism and epilepsy.</div></div>","PeriodicalId":54554,"journal":{"name":"Progress in Biophysics & Molecular Biology","volume":"198 ","pages":"Pages 21-31"},"PeriodicalIF":4.5,"publicationDate":"2025-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145071257","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}
Pub Date : 2025-09-06DOI: 10.1016/j.pbiomolbio.2025.09.001
Camilo Tayac , J. Torres-Osorio , José Mauricio Rodas-Rodríguez
The primary objective of this review is to analyze primary research published over the past six years concerning cyclic nucleotide-gated calcium channels (CNGC) in plants. The aim is to structure this information to identify and organize existing knowledge regarding their tertiary and quaternary structures, as well as the activation mechanisms of CNGC. Studies on plant CNGC published between January 2018 and May 2025 were included, while research focused on animals, bacteria, or ions other than calcium was excluded. Articles were retrieved from Scopus, Web of Science, and PubMed databases through searches conducted between June 2024 and May 2025, as well as from additional personal sources. A total of 111 articles met the inclusion criteria. These were categorized into seven groups: phylogenetic analysis and classification of plant CNGC monomers, gene expression regulation, structural composition of monomers and tetramers, channel activation, selectivity mechanisms, cellular localization, and the plant species and structural types in which they are found. The findings revealed that CNGC can be activated by individual mechanisms or by the interplay of multiple pathways. However, uncertainties remain regarding certain activation processes. A lack of experimental studies specifically aimed at elucidating their crystallographic structure was evident, which limits a comprehensive understanding of these channels and represents one of the main constraints of the available evidence. This limitation highlights the need for further research to fully elucidate both the activation mechanisms and structural characteristics of CNGC. Despite these constraints, the findings indicate that CNGC play a pivotal role in plant physiology.
本综述的主要目的是分析过去六年来发表的关于植物环核苷酸门控钙通道（CNGC）的初步研究。目的是组织这些信息，以识别和组织有关它们的三级和四级结构的现有知识，以及CNGC的激活机制。2018年1月至2025年5月期间发表的植物CNGC研究被纳入，而专注于动物、细菌或钙以外离子的研究被排除在外。文章通过2024年6月至2025年5月之间的搜索从Scopus、Web of Science和PubMed数据库检索，以及从其他个人来源检索。共有111篇文章符合纳入标准。主要包括植物CNGC单体的系统发育分析和分类、基因表达调控、单体和四聚体的结构组成、通道激活、选择性机制、细胞定位、植物种类和结构类型等7个方面。研究结果表明，CNGC可以通过个体机制或多种途径的相互作用激活。然而，某些激活过程仍然存在不确定性。缺乏专门旨在阐明其晶体结构的实验研究是显而易见的，这限制了对这些通道的全面理解，并代表了现有证据的主要限制之一。这一局限性表明，需要进一步研究以充分阐明CNGC的活化机制和结构特征。尽管存在这些限制，研究结果表明CNGC在植物生理中起着关键作用。
{"title":"Cationic calcium channels activated by cyclic nucleotides in plants: A systematic review using the PRISMA method","authors":"Camilo Tayac , J. Torres-Osorio , José Mauricio Rodas-Rodríguez","doi":"10.1016/j.pbiomolbio.2025.09.001","DOIUrl":"10.1016/j.pbiomolbio.2025.09.001","url":null,"abstract":"<div><div>The primary objective of this review is to analyze primary research published over the past six years concerning cyclic nucleotide-gated calcium channels (CNGC) in plants. The aim is to structure this information to identify and organize existing knowledge regarding their tertiary and quaternary structures, as well as the activation mechanisms of CNGC. Studies on plant CNGC published between January 2018 and May 2025 were included, while research focused on animals, bacteria, or ions other than calcium was excluded. Articles were retrieved from Scopus, Web of Science, and PubMed databases through searches conducted between June 2024 and May 2025, as well as from additional personal sources. A total of 111 articles met the inclusion criteria. These were categorized into seven groups: phylogenetic analysis and classification of plant CNGC monomers, gene expression regulation, structural composition of monomers and tetramers, channel activation, selectivity mechanisms, cellular localization, and the plant species and structural types in which they are found. The findings revealed that CNGC can be activated by individual mechanisms or by the interplay of multiple pathways. However, uncertainties remain regarding certain activation processes. A lack of experimental studies specifically aimed at elucidating their crystallographic structure was evident, which limits a comprehensive understanding of these channels and represents one of the main constraints of the available evidence. This limitation highlights the need for further research to fully elucidate both the activation mechanisms and structural characteristics of CNGC. Despite these constraints, the findings indicate that CNGC play a pivotal role in plant physiology.</div></div>","PeriodicalId":54554,"journal":{"name":"Progress in Biophysics & Molecular Biology","volume":"198 ","pages":"Pages 8-20"},"PeriodicalIF":4.5,"publicationDate":"2025-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145014478","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}
Pub Date : 2025-08-18DOI: 10.1016/j.pbiomolbio.2025.08.001
N.C. Ruppel, M.A. Model
The measurement of dry cell mass (often referred to as “protein”) under the microscope can be accomplished using a quantitative phase imaging technique known as Transport of Intensity Equation (TIE) microscopy. This method requires no specialized equipment, relying instead on two slightly defocused brightfield images acquired with a standard optical microscope. The images are processed by the TIE equation to convert the gradient of intensity into phase shifts and ultimately a distribution of protein mass. Beyond its simplicity, a major advantage of TIE over most other quantitative phase methods is its compatibility with fluorescence and with cell volume measurements. When paired with volume data, TIE enables the conversion of protein mass into the biologically significant parameters of protein concentration and intracellular water content.
This review emphasizes practical implementation, including calibration, focal plane selection, reproducibility, image size effects, strategies for artifact reduction, as well as the biological relevance of the recovered phase. We also describe an easy-to-use Fiji plugin for solving the TIE equation, eliminating the need for advanced computational tools.
{"title":"A guide to transport-of-intensity equation (TIE) imaging for biologists","authors":"N.C. Ruppel, M.A. Model","doi":"10.1016/j.pbiomolbio.2025.08.001","DOIUrl":"10.1016/j.pbiomolbio.2025.08.001","url":null,"abstract":"<div><div>The measurement of dry cell mass (often referred to as “protein”) under the microscope can be accomplished using a quantitative phase imaging technique known as Transport of Intensity Equation (TIE) microscopy. This method requires no specialized equipment, relying instead on two slightly defocused brightfield images acquired with a standard optical microscope. The images are processed by the TIE equation to convert the gradient of intensity into phase shifts and ultimately a distribution of protein mass. Beyond its simplicity, a major advantage of TIE over most other quantitative phase methods is its compatibility with fluorescence and with cell volume measurements. When paired with volume data, TIE enables the conversion of protein mass into the biologically significant parameters of protein concentration and intracellular water content.</div><div>This review emphasizes practical implementation, including calibration, focal plane selection, reproducibility, image size effects, strategies for artifact reduction, as well as the biological relevance of the recovered phase. We also describe an easy-to-use Fiji plugin for solving the TIE equation, eliminating the need for advanced computational tools.</div></div>","PeriodicalId":54554,"journal":{"name":"Progress in Biophysics & Molecular Biology","volume":"198 ","pages":"Pages 1-7"},"PeriodicalIF":4.5,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144889890","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}
Pub Date : 2025-08-01DOI: 10.1016/j.pbiomolbio.2025.07.004
Ildefonso M. De la Fuente , Jesus M. Cortes , Iker Malaina , Gorka Pérez-Yarza , Luis Martinez , José I. López , Maria Fedetz , Jose Carrasco-Pujante
{"title":"Corrigendum to “The main sources of molecular organization in the cell. Atlas of self-organized and self-regulated dynamic biostructures” [Prog. Biophys. Mol. Biol. 195 (2025) 167–191]","authors":"Ildefonso M. De la Fuente , Jesus M. Cortes , Iker Malaina , Gorka Pérez-Yarza , Luis Martinez , José I. López , Maria Fedetz , Jose Carrasco-Pujante","doi":"10.1016/j.pbiomolbio.2025.07.004","DOIUrl":"10.1016/j.pbiomolbio.2025.07.004","url":null,"abstract":"","PeriodicalId":54554,"journal":{"name":"Progress in Biophysics & Molecular Biology","volume":"197 ","pages":"Page 108"},"PeriodicalIF":4.5,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144750220","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}
Pub Date : 2025-07-21DOI: 10.1016/j.pbiomolbio.2025.07.005
Andrijana Angelovski , Markéta Bébarová
The microelectrode array (MEA) is an electronic device composed of a varying number of microelectrodes used to detect the extracellular field potential generated by excitable tissues. This technology allows for the measurement of electrical activity without damaging the cell membrane during recording. MEA offers a better way of getting long-term recordings and observing different cellular activities than the invasive patch clamp technique. Recent research demonstrates that MEA technology enables scientists to detect both cellular and subcellular events, allowing them to study cellular properties and reactions across different experimental conditions and even to identify distinct ion currents and their impact on cellular electrophysiology. The paper reviews the historical development of MEA technology along with its modern applications for electrophysiological research. The future advancement of MEA technology will improve our knowledge about neuronal and cardiac excitability and expand its use to additional electrically active tissues, advancing research in pharmacology, neuroscience, cardiology, and other fields.
{"title":"The microelectrode array technique - a crucial tool for studying excitable tissue disorders and drug testing: an update on recent advances","authors":"Andrijana Angelovski , Markéta Bébarová","doi":"10.1016/j.pbiomolbio.2025.07.005","DOIUrl":"10.1016/j.pbiomolbio.2025.07.005","url":null,"abstract":"<div><div>The microelectrode array (MEA) is an electronic device composed of a varying number of microelectrodes used to detect the extracellular field potential generated by excitable tissues. This technology allows for the measurement of electrical activity without damaging the cell membrane during recording. MEA offers a better way of getting long-term recordings and observing different cellular activities than the invasive patch clamp technique. Recent research demonstrates that MEA technology enables scientists to detect both cellular and subcellular events, allowing them to study cellular properties and reactions across different experimental conditions and even to identify distinct ion currents and their impact on cellular electrophysiology. The paper reviews the historical development of MEA technology along with its modern applications for electrophysiological research. The future advancement of MEA technology will improve our knowledge about neuronal and cardiac excitability and expand its use to additional electrically active tissues, advancing research in pharmacology, neuroscience, cardiology, and other fields.</div></div>","PeriodicalId":54554,"journal":{"name":"Progress in Biophysics & Molecular Biology","volume":"197 ","pages":"Pages 97-107"},"PeriodicalIF":4.5,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144700292","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}
Currently, computational protein design (CPD) is a disruptive force in biotechnology, changing the paradigm by which proteins are engineered for many applications. In this article, the evolution of CPD has been tracked from its initial forays in the late 1990s to the current advanced and sophisticated domain that it now occupies as one driven by artificial intelligence (AI). It highlights recent advancements that have extended its scope and into which broader elements including protein backbone modeling, energy functions, sampling algorithms, and techniques for sequence optimization were placed. Computer-aided protein design has thus become increasingly accurate and efficient through machine learning, quantum mechanics, and high-throughput virtual screening. In biotechnology, CPD finds applications in developing innovative therapeutics, industrial enzymes, and synthetic biomaterials. Such remarkable successes aside, however, CPD has various challenges, such as energy function, structural predictions, and computational resource requirements. Future predictions in areas such as programmable cellular systems and self-assembling protein-based materials could establish new avenues for growth. Finally, the review points out the need for multidisciplinarity and ethical considerations as well in utilizing CPD to reach its full potential for solving global issues of health, energy, and environmental sustainability. Having moved in that direction, CPD promises to open new avenues of biotechnological development that will enable the creation of proteins with functions and properties never before possible.
{"title":"Computational protein design: Advancing biotechnology through in silico engineering","authors":"Ranjit Ranbhor , Ruthvik Venkatesan , Amay Sanjay Redkar , Vibin Ramakrishnan","doi":"10.1016/j.pbiomolbio.2025.07.003","DOIUrl":"10.1016/j.pbiomolbio.2025.07.003","url":null,"abstract":"<div><div>Currently, computational protein design (CPD) is a disruptive force in biotechnology, changing the paradigm by which proteins are engineered for many applications. In this article, the evolution of CPD has been tracked from its initial forays in the late 1990s to the current advanced and sophisticated domain that it now occupies as one driven by artificial intelligence (AI). It highlights recent advancements that have extended its scope and into which broader elements including protein backbone modeling, energy functions, sampling algorithms, and techniques for sequence optimization were placed. Computer-aided protein design has thus become increasingly accurate and efficient through machine learning, quantum mechanics, and high-throughput virtual screening. In biotechnology, CPD finds applications in developing innovative therapeutics, industrial enzymes, and synthetic biomaterials. Such remarkable successes aside, however, CPD has various challenges, such as energy function, structural predictions, and computational resource requirements. Future predictions in areas such as programmable cellular systems and self-assembling protein-based materials could establish new avenues for growth. Finally, the review points out the need for multidisciplinarity and ethical considerations as well in utilizing CPD to reach its full potential for solving global issues of health, energy, and environmental sustainability. Having moved in that direction, CPD promises to open new avenues of biotechnological development that will enable the creation of proteins with functions and properties never before possible.</div></div>","PeriodicalId":54554,"journal":{"name":"Progress in Biophysics & Molecular Biology","volume":"197 ","pages":"Pages 75-83"},"PeriodicalIF":3.2,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144662684","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}
Pub Date : 2025-07-15DOI: 10.1016/j.pbiomolbio.2025.07.002
Xin Lan , Shuwen Zhang , Lu Yang
Taurine up-regulated 1 (TUG1) is a long non-coding RNA (lncRNA) that plays a significant role in the pathogenesis of both cancer and non-cancer diseases. Recent studies have revealed its involvement in regulating the development of various diseases by modulating the activity of the body's immune cells. In non-cancer diseases, TUG1 primarily influences disease progression through the competing endogenous RNA (ceRNA) network, promoting the expression of pro-inflammatory cytokines via pathways such as the NF-κB inflammatory signaling pathway. Most research indicates that TUG1 exerts a positive regulatory effect on immune cells, including Th2 cells, M1 macrophages, and microglia. In cancer, TUG1 regulates disease progression predominantly through the ceRNA network and by modulating the activity of specific transcription factors. It fosters tumor development by promoting the establishment of immune tolerance within the tumor microenvironment. This immune tolerance is associated with TUG1's regulation of immune checkpoint molecules, which enhances the infiltration of pro-tumor immune cells (e.g., regulatory T cells, M2 macrophages, neutrophils, and dendritic cells) while suppressing the infiltration of anti-tumor immune cells, including CD8+ T cells, NK cells, and M1 macrophages. In this study, we systematically evaluate the impact of abnormal TUG1 expression across various diseases, focusing on its mechanisms of action in regulating immune cell infiltration and disease progression in both cancer and non-cancer contexts. We also discuss potential targets for future research related to TUG1's role in these pathogenic processes.
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