Pub Date : 2026-01-02DOI: 10.1016/j.isci.2025.114621
Joan Giménez-Dejoz , Paula Vidal , Sonia Romero , David Almendral , Miguel Luengo , Mireia Martinez-Sugrañes , Jose L. Gonzalez-Alfonso , Ana Robles-Martín , Francisco J. Plou , Rafael Bargiela , Martin Floor , Manuel Ferrer , Víctor Guallar , Laura Fernandez-Lopez
Deep computationally guided protein design enabled the introduction of a Ser-His-Asp catalytic triad that supports polyethylene terephthalate (PET) hydrolysis within an inner membrane Escherichia coli protein. This allows the engineering, through gene editing, of a strain capable of degrading PET particles smaller than 4.5 nm. We extended this approach to PET powder (<300 μm) using a computational workflow that builds geometrically pre-organized catalytic triads while preserving substrate binding in extracellular or surface-exposed membrane proteins. Four additional proteins were reprogrammed to degrade PET. Replacement of the outer membrane protein OmpA with a PETase-active variant carrying a surface-exposed artificial triad enabled an engineered strain to release 157 ± 2 μM hydrolysis products within 24 h at 37°C and to sustain growth (0.18 ± 0.07 h−1) on PET powder as a carbon source. These results demonstrate the feasibility of engineering E. coli strains for PET powder biodegradation without exogenous PETase genes.
{"title":"Engineering Escherichia coli for polyethylene terephthalate powder biodegradation via recoding of an outer membrane protein","authors":"Joan Giménez-Dejoz , Paula Vidal , Sonia Romero , David Almendral , Miguel Luengo , Mireia Martinez-Sugrañes , Jose L. Gonzalez-Alfonso , Ana Robles-Martín , Francisco J. Plou , Rafael Bargiela , Martin Floor , Manuel Ferrer , Víctor Guallar , Laura Fernandez-Lopez","doi":"10.1016/j.isci.2025.114621","DOIUrl":"10.1016/j.isci.2025.114621","url":null,"abstract":"<div><div>Deep computationally guided protein design enabled the introduction of a Ser-His-Asp catalytic triad that supports polyethylene terephthalate (PET) hydrolysis within an inner membrane <em>Escherichia coli</em> protein. This allows the engineering, through gene editing, of a strain capable of degrading PET particles smaller than 4.5 nm. We extended this approach to PET powder (<300 μm) using a computational workflow that builds geometrically pre-organized catalytic triads while preserving substrate binding in extracellular or surface-exposed membrane proteins. Four additional proteins were reprogrammed to degrade PET. Replacement of the outer membrane protein OmpA with a PETase-active variant carrying a surface-exposed artificial triad enabled an engineered strain to release 157 ± 2 μM hydrolysis products within 24 h at 37°C and to sustain growth (0.18 ± 0.07 h<sup>−1</sup>) on PET powder as a carbon source. These results demonstrate the feasibility of engineering <em>E</em>. <em>coli</em> strains for PET powder biodegradation without exogenous PETase genes.</div></div>","PeriodicalId":342,"journal":{"name":"iScience","volume":"29 2","pages":"Article 114621"},"PeriodicalIF":4.1,"publicationDate":"2026-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146074772","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-02DOI: 10.1016/j.isci.2025.114610
Shiying Chen , Xiaofang Zhang , Tiantian Lu , Hui Lin , Xinrou Yu , Jun Wang , Dajun Lou , Dihua Huang
Diabetic cardiomyopathy (DCM) is a diabetes-specific cardiac dysfunction independent of other cardiovascular diseases. Recent studies highlight dysregulated fatty acid (FA) metabolism as a central driver of its pathogenesis. In the diabetic heart, excessive FA uptake and oxidation imbalance with glucose utilization led to lipid accumulation, mitochondrial overload, and oxidative stress. These changes trigger inflammatory responses, impair mitochondrial structural integrity and quality control, and disrupt cellular energy homeostasis. Over time, this maladaptation promotes cardiomyocyte hypertrophy, interstitial fibrosis, and progressive diastolic dysfunction. This review synthesizes current knowledge on the links between FA metabolic dysregulation and DCM, from metabolic overload to structural remodeling. It also discusses emerging therapeutic strategies aimed at reducing pathological lipid influx, optimizing energy substrate balance, restoring mitochondrial function, and preventing downstream injury, with the goal of guiding precision interventions for DCM.
{"title":"Integrative insights into fatty acid metabolism in diabetic cardiomyopathy: From molecular mechanisms to therapeutic strategies","authors":"Shiying Chen , Xiaofang Zhang , Tiantian Lu , Hui Lin , Xinrou Yu , Jun Wang , Dajun Lou , Dihua Huang","doi":"10.1016/j.isci.2025.114610","DOIUrl":"10.1016/j.isci.2025.114610","url":null,"abstract":"<div><div>Diabetic cardiomyopathy (DCM) is a diabetes-specific cardiac dysfunction independent of other cardiovascular diseases. Recent studies highlight dysregulated fatty acid (FA) metabolism as a central driver of its pathogenesis. In the diabetic heart, excessive FA uptake and oxidation imbalance with glucose utilization led to lipid accumulation, mitochondrial overload, and oxidative stress. These changes trigger inflammatory responses, impair mitochondrial structural integrity and quality control, and disrupt cellular energy homeostasis. Over time, this maladaptation promotes cardiomyocyte hypertrophy, interstitial fibrosis, and progressive diastolic dysfunction. This review synthesizes current knowledge on the links between FA metabolic dysregulation and DCM, from metabolic overload to structural remodeling. It also discusses emerging therapeutic strategies aimed at reducing pathological lipid influx, optimizing energy substrate balance, restoring mitochondrial function, and preventing downstream injury, with the goal of guiding precision interventions for DCM.</div></div>","PeriodicalId":342,"journal":{"name":"iScience","volume":"29 2","pages":"Article 114610"},"PeriodicalIF":4.1,"publicationDate":"2026-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145975110","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Emerging evidence suggests that maternal food intake and nutritional status may modify the relationship between environmental toxicants and early-life health risks, potentially mitigating their adverse effects. However, the interplay between nutritional status, environmental exposures, and health outcomes remains poorly characterized in the literature. Notably, foods can serve as the dual source of toxins (e.g., methylmercury in fish) and protective nutrients (e.g., omega-3 fatty acids), which complicate their role in risk reduction. This scoping review aims to evaluate the extent of research on how maternal nutrition (from both dietary intake and supplements) modify the risk of adverse early-life outcomes associated with environmental exposures. We also identified critical research gaps to guide future investigations. Our search included identified English-language, free full-text articles from PubMed and Google Scholar published up to November 2025. Among the 60 included studies (55 observational and 5 interventional), most were conducted in the USA (42%), with toxic metals (33%) and endocrine disrupting chemicals (EDCs) (20%) as the primary exposures. Folate (28%) and fish/fatty acids (15%) were the most frequently studied nutrients/food sources. Neurodevelopmental/behavioral disorders (42%) and adverse birth outcomes (32%) were the predominant endpoints. Maternal nutrition, particularly folate, fish, vitamins, and minerals, may mitigate environmental exposure-related risks. The findings suggest that folate may modify health risks from air pollution, toxic metals, and smoking, whereas fish intake, fatty acids, selenium, and vitamins A, B, C, D, and E may modify the effects of air pollution, EDCs, toxic metals, and smoking. Future research should prioritize mechanistic studies, optimal dosages, and longitudinal designs in diverse populations.
{"title":"Maternal environmental exposure and early-life health risks: The modulating role of nutritional status—A scoping review","authors":"Nida Shafiq , Chang Gao , Weitian Tang , Ruonan Li , Yichao Huang","doi":"10.1016/j.isci.2025.114606","DOIUrl":"10.1016/j.isci.2025.114606","url":null,"abstract":"<div><div>Emerging evidence suggests that maternal food intake and nutritional status may modify the relationship between environmental toxicants and early-life health risks, potentially mitigating their adverse effects. However, the interplay between nutritional status, environmental exposures, and health outcomes remains poorly characterized in the literature. Notably, foods can serve as the dual source of toxins (e.g., methylmercury in fish) and protective nutrients (e.g., omega-3 fatty acids), which complicate their role in risk reduction. This scoping review aims to evaluate the extent of research on how maternal nutrition (from both dietary intake and supplements) modify the risk of adverse early-life outcomes associated with environmental exposures. We also identified critical research gaps to guide future investigations. Our search included identified English-language, free full-text articles from PubMed and Google Scholar published up to November 2025. Among the 60 included studies (55 observational and 5 interventional), most were conducted in the USA (42%), with toxic metals (33%) and endocrine disrupting chemicals (EDCs) (20%) as the primary exposures. Folate (28%) and fish/fatty acids (15%) were the most frequently studied nutrients/food sources. Neurodevelopmental/behavioral disorders (42%) and adverse birth outcomes (32%) were the predominant endpoints. Maternal nutrition, particularly folate, fish, vitamins, and minerals, may mitigate environmental exposure-related risks. The findings suggest that folate may modify health risks from air pollution, toxic metals, and smoking, whereas fish intake, fatty acids, selenium, and vitamins A, B, C, D, and E may modify the effects of air pollution, EDCs, toxic metals, and smoking. Future research should prioritize mechanistic studies, optimal dosages, and longitudinal designs in diverse populations.</div></div>","PeriodicalId":342,"journal":{"name":"iScience","volume":"29 2","pages":"Article 114606"},"PeriodicalIF":4.1,"publicationDate":"2026-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146035712","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-02DOI: 10.1016/j.isci.2025.114608
Neema Jamshidi , Katharina von Löhneysen , Katrin Soldau , Jeffrey S. Friedman
Biochemical aging involves progressive declines in energy metabolism and redox maintenance. The peroxiredoxin enzyme family is critical for maintenance of cellular redox states. In mice, enucleate mature red blood cells (RBCs) persist for roughly 50 days, providing an ideal system for tracking cellular aging in vivo. To define the impact of impaired redox function, we analyzed the RBC metabolome across defined cellular ages using biotin labeling to isolate populations at approximately 1, 2, and 3 weeks. A total of 183 metabolites were quantified by mass spectrometry. Overall metabolic trajectories were similar between wild-type and Prdx2-deficient RBCs, with age-associated shifts involving ATP-generating pathways, redox maintenance processes, and membrane-structure-related reactions. However, these metabolic changes were consistently more pronounced in Prdx2 knockout RBCs, indicating accelerated disruption of pathways linked to energy production and redox balance. These findings indicate that Prdx2 is essential for maintaining metabolic homeostasis during RBC aging.
{"title":"The loss of peroxiredoxin 2 in mice disrupts the biochemical aging phenotype in erythrocytes","authors":"Neema Jamshidi , Katharina von Löhneysen , Katrin Soldau , Jeffrey S. Friedman","doi":"10.1016/j.isci.2025.114608","DOIUrl":"10.1016/j.isci.2025.114608","url":null,"abstract":"<div><div>Biochemical aging involves progressive declines in energy metabolism and redox maintenance. The peroxiredoxin enzyme family is critical for maintenance of cellular redox states. In mice, enucleate mature red blood cells (RBCs) persist for roughly 50 days, providing an ideal system for tracking cellular aging <em>in vivo</em>. To define the impact of impaired redox function, we analyzed the RBC metabolome across defined cellular ages using biotin labeling to isolate populations at approximately 1, 2, and 3 weeks. A total of 183 metabolites were quantified by mass spectrometry. Overall metabolic trajectories were similar between wild-type and Prdx2-deficient RBCs, with age-associated shifts involving ATP-generating pathways, redox maintenance processes, and membrane-structure-related reactions. However, these metabolic changes were consistently more pronounced in Prdx2 knockout RBCs, indicating accelerated disruption of pathways linked to energy production and redox balance. These findings indicate that Prdx2 is essential for maintaining metabolic homeostasis during RBC aging.</div></div>","PeriodicalId":342,"journal":{"name":"iScience","volume":"29 2","pages":"Article 114608"},"PeriodicalIF":4.1,"publicationDate":"2026-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146035796","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-02DOI: 10.1016/j.isci.2025.114596
Ling Lian , Hayley Robinson , Noah Daniels , G. Aleph Prieto , Gunnar H.D. Poplawski , Rodrigo Lopez-Gonzalez
The C9orf72 hexanucleotide repeat expansion (G4C2) is the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), yet targeted therapies remain unavailable. Here, we show that induced pluripotent stem cell (iPSC)-derived post-mitotic neurons from C9orf72 carriers exhibit age-dependent cell-cycle reentry, increased S-phase entry, and elevated cyclin and CDK expression. Mechanistically, arginine-containing dipeptide repeat proteins (poly-GR and poly-PR) translated from G4C2 repeats drive this aberrant activation through stimulation of the CDK4/6 pathway, whereas poly-GP and C9orf72 loss-of-function show no effect. Importantly, the FDA-approved CDK4/6 inhibitor palbociclib normalizes cell-cycle progression, reduces S-phase entry, decreases motor neuron death, and restores synaptic proteins PSD95 and synapsin-1. Single-nucleus RNA sequencing from C9orf72 patient cortex reveals cell-cycle activation within excitatory neuron subclusters and alterations in DNA repair and cell-cycle regulation pathways, supporting our in vitro findings. These findings establish cell-cycle dysregulation as a central pathogenic mechanism in C9orf72 ALS/FTD and highlight CDK4/6 signaling as a promising therapeutic target.
{"title":"Aberrant CDK4/6-driven cell-cycle reentry drives neuronal loss and defines a therapeutic target in C9orf72 ALS/FTD","authors":"Ling Lian , Hayley Robinson , Noah Daniels , G. Aleph Prieto , Gunnar H.D. Poplawski , Rodrigo Lopez-Gonzalez","doi":"10.1016/j.isci.2025.114596","DOIUrl":"10.1016/j.isci.2025.114596","url":null,"abstract":"<div><div>The C9orf72 hexanucleotide repeat expansion (G4C2) is the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), yet targeted therapies remain unavailable. Here, we show that induced pluripotent stem cell (iPSC)-derived post-mitotic neurons from C9orf72 carriers exhibit age-dependent cell-cycle reentry, increased S-phase entry, and elevated cyclin and CDK expression. Mechanistically, arginine-containing dipeptide repeat proteins (poly-GR and poly-PR) translated from G4C2 repeats drive this aberrant activation through stimulation of the CDK4/6 pathway, whereas poly-GP and C9orf72 loss-of-function show no effect. Importantly, the FDA-approved CDK4/6 inhibitor palbociclib normalizes cell-cycle progression, reduces S-phase entry, decreases motor neuron death, and restores synaptic proteins PSD95 and synapsin-1. Single-nucleus RNA sequencing from C9orf72 patient cortex reveals cell-cycle activation within excitatory neuron subclusters and alterations in DNA repair and cell-cycle regulation pathways, supporting our <em>in vitro</em> findings. These findings establish cell-cycle dysregulation as a central pathogenic mechanism in C9orf72 ALS/FTD and highlight CDK4/6 signaling as a promising therapeutic target.</div></div>","PeriodicalId":342,"journal":{"name":"iScience","volume":"29 2","pages":"Article 114596"},"PeriodicalIF":4.1,"publicationDate":"2026-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146035864","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-02DOI: 10.1016/j.isci.2025.114618
Mingshuang Tang , Huijie Cui , Xueyao Wu , Yutong Wang , Xunying Zhao , Rong Xiang , Jinyu Xiao , Lin Chen , Yanqiu Zou , Yunjie Liu , BoWen Lei , Xiaofeng Ma , Di Zhang , Mengyu Fan , Jiayuan Li , Xia Jiang , Ben Zhang
To investigate the roles of immune cells in cancer, we conducted Mendelian randomization (MR) analyses of 731 immune cells and 16 site-specific cancers, alongside gene-based and enrichment analyses. MR identified 79 significant associations (46 protective, 33 risk-enhancing). Key findings include BAFF-R on B cells lowering melanoma risk, and CD27 on B cells increasing lung cancer risk. Associations were also observed with breast, ovarian, cervical, and other cancers, but no significant association was found with oral cavity or pancreatic cancers. Gene-based analysis revealed 61 shared genes between immune cells and cancers. 56 genes were associated with prostate cancer, 30 with lung cancer, three with breast cancer, two with cervical cancer, and one with melanoma. Interestingly, several prostate cancer-associated genes were also associated with breast, cervical, and lung cancers. These findings suggest potential biological mechanisms linking immune cells to cancer development and progression, highlighting the complex role of the immune system in cancer.
{"title":"Association between immune cells and multiple cancers: Insights from Mendelian randomization and gene-based analysis","authors":"Mingshuang Tang , Huijie Cui , Xueyao Wu , Yutong Wang , Xunying Zhao , Rong Xiang , Jinyu Xiao , Lin Chen , Yanqiu Zou , Yunjie Liu , BoWen Lei , Xiaofeng Ma , Di Zhang , Mengyu Fan , Jiayuan Li , Xia Jiang , Ben Zhang","doi":"10.1016/j.isci.2025.114618","DOIUrl":"10.1016/j.isci.2025.114618","url":null,"abstract":"<div><div>To investigate the roles of immune cells in cancer, we conducted Mendelian randomization (MR) analyses of 731 immune cells and 16 site-specific cancers, alongside gene-based and enrichment analyses. MR identified 79 significant associations (46 protective, 33 risk-enhancing). Key findings include BAFF-R on B cells lowering melanoma risk, and CD27 on B cells increasing lung cancer risk. Associations were also observed with breast, ovarian, cervical, and other cancers, but no significant association was found with oral cavity or pancreatic cancers. Gene-based analysis revealed 61 shared genes between immune cells and cancers. 56 genes were associated with prostate cancer, 30 with lung cancer, three with breast cancer, two with cervical cancer, and one with melanoma. Interestingly, several prostate cancer-associated genes were also associated with breast, cervical, and lung cancers. These findings suggest potential biological mechanisms linking immune cells to cancer development and progression, highlighting the complex role of the immune system in cancer.</div></div>","PeriodicalId":342,"journal":{"name":"iScience","volume":"29 2","pages":"Article 114618"},"PeriodicalIF":4.1,"publicationDate":"2026-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146035869","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-31DOI: 10.1016/j.isci.2025.114600
Zhiqi Zhang , Xiangdong Sun , Jianxiang Shi , Hongen Xu , Haoyu Wang , Zhaohui Yang , Jiancheng Guo , Zengguang Yang , Chenxi Li , Jicun Zhu , Yuexiao Zhang , Pengyuan Zheng , Xia Xue , Yang Mi
The attrition of telomere length is associated with cellular aging and plays a role in multiple age-related disorders. This study analyzed the relationship between telomere length on the X chromosome and age in the Han population (n = 492) using whole-genome sequencing and long-read sequencing data from 32 individuals. We developed three pairs of primers and completed measurements in a cohort of 124 individuals. We then constructed an online prediction tool based on a three-layer feedforward neural network and validated its performance in an independent cohort of 41 individuals. Our results revealed a complex association between X chromosome telomere length and aging. No significant changes were observed in individuals under 30, while a significant negative correlation emerged in the population over 40, suggesting a potential “telomere shortening accelerating point (TSAP)” around this age. This finding challenges the conventional view of linear telomere shortening, and our model provides effective tools for exploring aging mechanisms.
{"title":"Optimized primer and model improve precision of X chromosome telomere length determination in the Han population","authors":"Zhiqi Zhang , Xiangdong Sun , Jianxiang Shi , Hongen Xu , Haoyu Wang , Zhaohui Yang , Jiancheng Guo , Zengguang Yang , Chenxi Li , Jicun Zhu , Yuexiao Zhang , Pengyuan Zheng , Xia Xue , Yang Mi","doi":"10.1016/j.isci.2025.114600","DOIUrl":"10.1016/j.isci.2025.114600","url":null,"abstract":"<div><div>The attrition of telomere length is associated with cellular aging and plays a role in multiple age-related disorders. This study analyzed the relationship between telomere length on the X chromosome and age in the Han population (<em>n</em> = 492) using whole-genome sequencing and long-read sequencing data from 32 individuals. We developed three pairs of primers and completed measurements in a cohort of 124 individuals. We then constructed an online prediction tool based on a three-layer feedforward neural network and validated its performance in an independent cohort of 41 individuals. Our results revealed a complex association between X chromosome telomere length and aging. No significant changes were observed in individuals under 30, while a significant negative correlation emerged in the population over 40, suggesting a potential “telomere shortening accelerating point (TSAP)” around this age. This finding challenges the conventional view of linear telomere shortening, and our model provides effective tools for exploring aging mechanisms.</div></div>","PeriodicalId":342,"journal":{"name":"iScience","volume":"29 2","pages":"Article 114600"},"PeriodicalIF":4.1,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145975711","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-31DOI: 10.1016/j.isci.2025.114550
Han-Ping Wang , Chen-Yu Xu , Wen Su , Yin-Song Wang , Yue Wang , Ming-Xin Cao
Periodontitis is a chronic inflammatory disease that leads to periodontal attachment loss and is a major cause of adult tooth loss. Current treatment of mechanical debridement is often ineffective in deep periodontal pockets, and antibiotic adjuncts carry the risk of bacterial resistance. Octyl gallate (OG), a natural plant-derived compound with antibacterial and antioxidant properties, is limited by poor water solubility and stability. This study aimed to develop a sustained-release ointment (OG-Ointment) using Pluronic F127 and ethylcellulose to enhance the delivery and efficacy of OG. The formulated OG-Ointment demonstrated excellent rheological properties, sustained drug release, and potent ABTS+ radical scavenging. In vitro, it enhanced bacterial membrane permeability, inhibited P. gingivalis growth, and reduced ROS in macrophages. In a rat periodontitis model, OG-Ointment significantly reduced alveolar bone resorption, decreased ROS and inflammatory cytokines, and exhibited good biocompatibility. These findings suggest that OG-Ointment is a promising non-antibiotic adjunctive therapy for periodontitis, combining dual antioxidant and antibacterial functions with sustained release.
{"title":"An antioxidant and antibacterial octyl gallate sustained-release ointment for periodontitis treatment","authors":"Han-Ping Wang , Chen-Yu Xu , Wen Su , Yin-Song Wang , Yue Wang , Ming-Xin Cao","doi":"10.1016/j.isci.2025.114550","DOIUrl":"10.1016/j.isci.2025.114550","url":null,"abstract":"<div><div>Periodontitis is a chronic inflammatory disease that leads to periodontal attachment loss and is a major cause of adult tooth loss. Current treatment of mechanical debridement is often ineffective in deep periodontal pockets, and antibiotic adjuncts carry the risk of bacterial resistance. Octyl gallate (OG), a natural plant-derived compound with antibacterial and antioxidant properties, is limited by poor water solubility and stability. This study aimed to develop a sustained-release ointment (OG-Ointment) using Pluronic F127 and ethylcellulose to enhance the delivery and efficacy of OG. The formulated OG-Ointment demonstrated excellent rheological properties, sustained drug release, and potent ABTS<sup>+</sup> radical scavenging. <em>In vitro</em>, it enhanced bacterial membrane permeability, inhibited <em>P. gingivalis</em> growth, and reduced ROS in macrophages. In a rat periodontitis model, OG-Ointment significantly reduced alveolar bone resorption, decreased ROS and inflammatory cytokines, and exhibited good biocompatibility. These findings suggest that OG-Ointment is a promising non-antibiotic adjunctive therapy for periodontitis, combining dual antioxidant and antibacterial functions with sustained release.</div></div>","PeriodicalId":342,"journal":{"name":"iScience","volume":"29 2","pages":"Article 114550"},"PeriodicalIF":4.1,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145975714","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-31DOI: 10.1016/j.isci.2025.114593
Rodolphe Thiébaut , Edouard Lhomme , Hakim Hocini , Isabelle Pellegrin , Andrea Boizard-Moracchini , Alexandre Duvignaud , Maud Perpère , Mélanie Huchon , Mélanie Prague , Christine Lacabaratz , Mathieu Surenaud , Xavier Anglaret , Denis Malvy , Boris P. Hejblum , Yves Levy , COVERAGE study group
Whole-blood gene expression analysis is essential for understanding molecular host responses, yet its use typically relies on venous sampling, limiting feasibility for frequent and remote monitoring. In an ancillary study of the COVERAGE France platform trial (NCT04356495), which enrolled at-risk outpatients with mild coronavirus disease 2019 (COVID-19) monitored at home, we compared transcriptomic profiles obtained from paired venous blood (Tempus tubes) and ultralow-volume, self-collected finger-prick capillary samples. We observed moderate to good concordance at the individual gene level and excellent agreement at the gene-set level between the two sampling approaches. High-frequency finger-prick sampling enabled daily resolution of immune dynamics, revealing early interferon responses, sustained neutrophil activation, and evolving erythroid and inflammatory signatures during the initial phase of mild COVID-19. These results demonstrate that finger-prick sampling is a feasible and reliable approach for at-home transcriptomic profiling, offering a powerful tool for longitudinal immune monitoring and advanced clinical research.
{"title":"Self-collected finger-prick blood for gene expression profiling: Unveiling early immune responses in mild COVID-19","authors":"Rodolphe Thiébaut , Edouard Lhomme , Hakim Hocini , Isabelle Pellegrin , Andrea Boizard-Moracchini , Alexandre Duvignaud , Maud Perpère , Mélanie Huchon , Mélanie Prague , Christine Lacabaratz , Mathieu Surenaud , Xavier Anglaret , Denis Malvy , Boris P. Hejblum , Yves Levy , COVERAGE study group","doi":"10.1016/j.isci.2025.114593","DOIUrl":"10.1016/j.isci.2025.114593","url":null,"abstract":"<div><div>Whole-blood gene expression analysis is essential for understanding molecular host responses, yet its use typically relies on venous sampling, limiting feasibility for frequent and remote monitoring. In an ancillary study of the COVERAGE France platform trial (<span><span>NCT04356495</span><svg><path></path></svg></span>), which enrolled at-risk outpatients with mild coronavirus disease 2019 (COVID-19) monitored at home, we compared transcriptomic profiles obtained from paired venous blood (Tempus tubes) and ultralow-volume, self-collected finger-prick capillary samples. We observed moderate to good concordance at the individual gene level and excellent agreement at the gene-set level between the two sampling approaches. High-frequency finger-prick sampling enabled daily resolution of immune dynamics, revealing early interferon responses, sustained neutrophil activation, and evolving erythroid and inflammatory signatures during the initial phase of mild COVID-19. These results demonstrate that finger-prick sampling is a feasible and reliable approach for at-home transcriptomic profiling, offering a powerful tool for longitudinal immune monitoring and advanced clinical research.</div></div>","PeriodicalId":342,"journal":{"name":"iScience","volume":"29 2","pages":"Article 114593"},"PeriodicalIF":4.1,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146035788","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-31DOI: 10.1016/j.isci.2025.114594
Nadiia Chernobai , Nadiia Shevchenko , Igor Kovalenko , Leonid Rozanov
The study of osmotic reactions of cells during freezing and thawing is a crucial topic requiring detailed investigation. Understanding these processes allows for the optimization of cryopreservation protocols, thereby improving cell survival after thawing. While the literature provides information on the osmotic characteristics of various mammalian cells, data on plant cells, including microalgae, remain scarce. This article examines the osmotic behavior of microalgae cells, which are promising from a biotechnological perspective, during freezing and thawing. We obtained results on the osmotically inactive cell volume and, using a physical-mathematical model, determined the permeability coefficients of cells for water and cryoprotectants. These results will be used in further work on developing cryopreservation protocols for microalgae, enabling the optimization of the process and achieving the best possible post-thaw survival outcomes.
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