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The therapeutic opportunities and pitfalls of using iron ion chelators to treat neurodegenerative diseases 使用铁离子螯合剂治疗神经退行性疾病的治疗机会和缺陷。
IF 3 4区 生物学
FEBS Letters Pub Date : 2026-08-24 Epub Date: 2026-07-25 DOI: 10.1002/1873-3468.70415
Barry Halliwell
{"title":"The therapeutic opportunities and pitfalls of using iron ion chelators to treat neurodegenerative diseases","authors":"Barry Halliwell","doi":"10.1002/1873-3468.70415","DOIUrl":"10.1002/1873-3468.70415","url":null,"abstract":"<p>There is considerable evidence that iron accumulation in the affected brain regions plays a role in the pathology of neurodegenerative diseases, probably because of the ability of iron ions to promote oxidative damage to important biomolecules, such as DNA, RNA, proteins and lipids (leading to lipid peroxidation). Yet recent clinical trials of iron ion-chelating agents in human neurodegenerative diseases have given unimpressive results, in several cases making the diseases worse. In using iron chelators, it is important to remember the basics of their redox chemistry, which could explain their lack of therapeutic effects. This issue is explored here, and the potential of iron ion chelation in the treatment of neurodegeneration is critically evaluated.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"600 16","pages":"2219-2225"},"PeriodicalIF":3.0,"publicationDate":"2026-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/1873-3468.70415","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148590907","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Partial depletion of plasminogen activator inhibitor-1 decreases subcutaneous fat cell hypertrophy and liver cholesterol in high-fat-fed female mice. 部分消耗纤溶酶原激活物抑制剂-1可减少高脂喂养雌性小鼠皮下脂肪细胞肥大和肝脏胆固醇。
IF 3 4区 生物学
FEBS Letters Pub Date : 2026-08-21 DOI: 10.1002/1873-3468.70439
Claudia E Ramirez Bustamante, Robert Sharp, Pradip K Saha, Elizabeth S Anaya, Elizabeth L Lieu, Evelyn L de Groot, Pooja Patel, Mi Jeong Heo, Aaron R Cox, Kang Ho Kim, Sean M Hartig
{"title":"Partial depletion of plasminogen activator inhibitor-1 decreases subcutaneous fat cell hypertrophy and liver cholesterol in high-fat-fed female mice.","authors":"Claudia E Ramirez Bustamante, Robert Sharp, Pradip K Saha, Elizabeth S Anaya, Elizabeth L Lieu, Evelyn L de Groot, Pooja Patel, Mi Jeong Heo, Aaron R Cox, Kang Ho Kim, Sean M Hartig","doi":"10.1002/1873-3468.70439","DOIUrl":"10.1002/1873-3468.70439","url":null,"abstract":"<p><p>Higher levels of plasminogen activator inhibitor-1 (PAI-1) circulate in the blood of people with obesity and predict hyperlipidemia and metabolic dysfunction-associated steatotic liver disease in studies predominantly conducted in women. To understand the roles of PAI-1 in women with obesity, we generated inducible whole-body PAI-1-depleted female mice (Pai-1<sup>i-KD</sup>). After high-fat diet feeding, Pai-1<sup>i-KD</sup> and littermate controls did not differ in body weight or energy balance. However, Pai-1<sup>i-KD</sup> females accumulated smaller inguinal WAT adipocytes. Spectral flow cytometry revealed reduced adipocyte progenitors and macrophages in inguinal WAT. Pai-1<sup>i-KD</sup> mice also exhibited decreased liver cholesterol. These preclinical findings argue that elevated PAI-1 alters subcutaneous adipose tissue biology and contributes to pathogenic phenotypes of obesity.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148790139","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Ligand-dependent transcriptional heterogeneity in cell cycle gene expression delays G1/S entry. 细胞周期基因表达中的配体依赖性转录异质性延迟G1/S进入。
IF 3 4区 生物学
FEBS Letters Pub Date : 2026-08-21 DOI: 10.1002/1873-3468.70440
Ririn Rahmala Febri, Ayaka Nagasato-Ichikawa, Keita Iida, Shuhei Kimura, Akira Imamoto, Mariko Okada
{"title":"Ligand-dependent transcriptional heterogeneity in cell cycle gene expression delays G1/S entry.","authors":"Ririn Rahmala Febri, Ayaka Nagasato-Ichikawa, Keita Iida, Shuhei Kimura, Akira Imamoto, Mariko Okada","doi":"10.1002/1873-3468.70440","DOIUrl":"https://doi.org/10.1002/1873-3468.70440","url":null,"abstract":"<p><p>ErbB ligands activate distinct receptor dimers that regulate cell proliferation, but how they influence cell-cycle commitment remains unclear. Here, we show that EGF and HRG induce different modes of G1/S progression in ErbB2-amplified BT474 breast cancer cells. Unexpectedly, HRG, despite activating the more potent ErbB2-ErbB3 heterodimer, failed to accelerate G1/S progression; instead, EGF promoted earlier passage through the restriction point and faster S-phase entry. Mechanistically, EGF drove rapid and coordinated cell-cycle progression through ERK-FOS signaling, whereas HRG induced sustained MYC activity, elevated transcriptional heterogeneity, and caused extensive rewiring of cell-cycle regulatory networks. Together, these findings reveal that ligand-specific ErbB signaling controls not only the timing of cell-cycle entry but also the transcriptional architecture that governs proliferative fate decisions.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148790192","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
The impact of aging on the gut-liver axis in health and disease. 衰老对肠肝轴在健康与疾病中的影响。
IF 3 4区 生物学
FEBS Letters Pub Date : 2026-08-20 DOI: 10.1002/1873-3468.70445
Konstancja Gałat, Natalia Rzepka, Aleksandra A Kołodziejczyk
{"title":"The impact of aging on the gut-liver axis in health and disease.","authors":"Konstancja Gałat, Natalia Rzepka, Aleksandra A Kołodziejczyk","doi":"10.1002/1873-3468.70445","DOIUrl":"https://doi.org/10.1002/1873-3468.70445","url":null,"abstract":"<p><p>Aging is a complex biological process characterized by gradual impairment of organ function and increased susceptibility to disease. Among the systems most affected, the gut and liver are particularly important because of their role in metabolism, detoxification, and immune regulation. These two organs are closely connected through the portal vein and bile ducts, enabling continuous, bidirectional communication that coordinates homeostasis. Understanding how gut-liver communication changes with age is therefore critical, as even subtle alterations over time can have widespread effects on overall physiology and the progression of age-related disorders. In this review, we examine current knowledge on how aging shapes gut and liver physiology, highlighting changes in microbial composition, barrier function, and hepatic metabolism. We then discuss how sex influences the gut-liver axis during aging. Finally, we explore how disruptions in the gut-liver axis contribute to the development of age-related conditions.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148790179","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Oxidative modification of the D1 residue 332H during photoinactivation drives photosystem II turnover. 在光失活过程中D1残基332H的氧化修饰驱动光系统II的更新。
IF 3 4区 生物学
FEBS Letters Pub Date : 2026-08-19 DOI: 10.1002/1873-3468.70431
Terry M Bricker, Laurie K Frankel
{"title":"Oxidative modification of the D1 residue <sup>332</sup>H during photoinactivation drives photosystem II turnover.","authors":"Terry M Bricker, Laurie K Frankel","doi":"10.1002/1873-3468.70431","DOIUrl":"https://doi.org/10.1002/1873-3468.70431","url":null,"abstract":"<p><p>Photosystem II (PS II) is a water-plastoquinone oxidoreductase. This photosystem has a short half-life (< 1 h) which is driven by repair of oxidative damage to the D1 protein. Reactive oxygen species (ROS) produced by the photosystem under stress conditions oxidatively modify key residues, which trigger the sequential disassembly of the photosystem. We hypothesize that the principal target for ROS damage of D1 is <sup>332</sup>His. This residue is a ligand to Mn1 of the Mn<sub>4</sub>CaO<sub>5</sub> cluster and is the first residue exhibiting oxidative modification during photoinactivation. Recently, cryo-EM studies indicate that PS II monomers containing oxidatively modified <sup>332</sup>His lose their manganese clusters and the extrinsic proteins associated with the photosystem, both hallmarks of the earliest stages of PS II turnover/repair.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148790136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Autophagy and mitophagy in pancreatic β-cell homeostasis and their involvement in diabetes pathophysiology. 胰腺β细胞稳态中的自噬和有丝自噬及其在糖尿病病理生理中的作用。
IF 3 4区 生物学
FEBS Letters Pub Date : 2026-08-19 DOI: 10.1002/1873-3468.70436
Yunkyeong Lee, Mingming Tong, Anna L Gloyn
{"title":"Autophagy and mitophagy in pancreatic β-cell homeostasis and their involvement in diabetes pathophysiology.","authors":"Yunkyeong Lee, Mingming Tong, Anna L Gloyn","doi":"10.1002/1873-3468.70436","DOIUrl":"https://doi.org/10.1002/1873-3468.70436","url":null,"abstract":"<p><p>Autophagy is an evolutionarily conserved cellular quality control pathway that responds to the metabolic state of the cell, and its dysregulation has been broadly associated with metabolic disorders like diabetes mellitus. Among different types of autophagy, mitophagy or the selective autophagic clearance of dysfunctional mitochondria has emerged as particularly relevant in pancreatic β-cell biology and its pathophysiology. Recent advances in functional genomics and animal studies implicate the autophagy/mitophagy pathway components as effector transcripts at diabetes risk loci, providing a new rationale for investigation of genetic determinants of autophagy/mitophagy in β cells. In this review, we take a β-cell centric perspective to examine the evidence for autophagy/mitophagy across four clinically relevant diabetes categories (type 1, type 2, gestational, and monogenic diabetes) and discuss the functional significance and complexity of these pathways in β-cell failure.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148790209","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Synergistic perspectives-How single-molecule biophysics complement biochemical understanding. 协同视角-单分子生物物理学如何补充生化理解。
IF 3 4区 生物学
FEBS Letters Pub Date : 2026-08-19 DOI: 10.1002/1873-3468.70444
Sara De Bragança, Eline L Jansen, Jorine M Eeftens
{"title":"Synergistic perspectives-How single-molecule biophysics complement biochemical understanding.","authors":"Sara De Bragança, Eline L Jansen, Jorine M Eeftens","doi":"10.1002/1873-3468.70444","DOIUrl":"https://doi.org/10.1002/1873-3468.70444","url":null,"abstract":"<p><p>Single-molecule biophysical techniques enable the study of biological systems by directly observing individual molecules and events, rather than measuring population averages. These approaches reveal transient states, rare events, conformational dynamics, and subpopulations that are often obscured in biochemical assays. The application of single-molecule methods has been limited by technical complexity and the need for specialized instrumentation. Recent standardization of protocols, methodologies, and platforms has lowered these barriers, enabling broader adoption and promoting interdisciplinary collaborations that facilitate integration into biochemical research. In this review, we discuss how ensemble biochemistry and single-molecule approaches are complementary, outline commonly used single-molecule techniques, and illustrate their relevance through two representative case studies: chromatin organization by SMC complexes and pathway choice during DNA double-strand break repair.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148790174","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Divergent effects of copper and cisplatin on the endocytic trafficking of copper transporter-1. 铜和顺铂对铜转运蛋白1内吞运输的不同影响。
IF 3 4区 生物学
FEBS Letters Pub Date : 2026-08-18 DOI: 10.1002/1873-3468.70441
Mainak Chakraborty, Swastika Dey, Sumanta Kar, Arnab Gupta
{"title":"Divergent effects of copper and cisplatin on the endocytic trafficking of copper transporter-1.","authors":"Mainak Chakraborty, Swastika Dey, Sumanta Kar, Arnab Gupta","doi":"10.1002/1873-3468.70441","DOIUrl":"https://doi.org/10.1002/1873-3468.70441","url":null,"abstract":"<p><p>Cisplatin (CDDP), a widely used chemotherapeutic agent, enters mammalian cells through high-affinity copper transporter CTR1. We found that copper preloading reduces CDDP cytotoxicity, supporting a shared uptake mechanism for copper and cisplatin. CDDP-induced CTR1 endocytosis requires both the amino-terminal His-Met motifs and the conserved 150MXXM154 pore-motif, similar to copper-mediated transport. Following internalization, CTR1 is routed through VPS35-positive endosomes and ultimately targeted to lysosomes. However, unlike copper, CDDP suppresses local recycling of CTR1 to plasma membrane and delays its lysosomal delivery. While copper promotes rapid lysosomal clearance of CTR1, CDDP results in prolonged intracellular trafficking. Additionally, CDDP enhances lysosomal size and cathepsin activity, indicating lysosomal activation. These findings reveal distinct mechanisms underlying CTR1-mediated cisplatin uptake and its impact on lysosomal physiology.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148790197","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Computational navigation of constrained multidimensional protein fitness landscapes. 约束多维蛋白质适应度景观的计算导航。
IF 3 4区 生物学
FEBS Letters Pub Date : 2026-08-17 DOI: 10.1002/1873-3468.70442
Rahul Kaushik, Firoozeh Piroozmand, Suyong Re
{"title":"Computational navigation of constrained multidimensional protein fitness landscapes.","authors":"Rahul Kaushik, Firoozeh Piroozmand, Suyong Re","doi":"10.1002/1873-3468.70442","DOIUrl":"https://doi.org/10.1002/1873-3468.70442","url":null,"abstract":"<p><p>Protein engineering relies heavily on computational characterization of constrained protein fitness landscapes, in which only a limited fraction of sequence space corresponds to stable and functional biomolecules. Advances in structural biology and machine learning are progressively shifting protein design strategies from empirical optimization toward multidimensional evaluation of sequence-structure-function relationships. This review examines current computational strategies for exploring these landscapes, including sequence-derived evolutionary descriptors, structural fitness assessment, energetic evaluation, and integrated multi-parameter scoring. Recent developments in protein language models, deep-learning-based structure prediction, generative protein design, and consensus scoring approaches support large-scale exploration of biologically accessible sequence space. Negative-design constraints, including aggregation propensity, intrinsic disorder, and developability are important in prioritizing experimentally tractable protein candidates. Finally, the integration of computational prediction with iterative experimental validation is discussed as a central framework for rational protein engineering. By framing structure prediction, sequence representation learning, and generative design as complementary strategies for navigating a single constrained fitness landscape, this review highlights integrated, multidimensional scoring and negative-design filtering as the critical link between computational candidate generation and experimentally tractable protein design.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148758496","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
The microbiome in human skin aging. 微生物群在人体皮肤老化中的作用。
IF 3 4区 生物学
FEBS Letters Pub Date : 2026-08-15 DOI: 10.1002/1873-3468.70435
Manuel Huerta Arana, Cornelia Wiegand, Omid Omrani, Mario Fabri
{"title":"The microbiome in human skin aging.","authors":"Manuel Huerta Arana, Cornelia Wiegand, Omid Omrani, Mario Fabri","doi":"10.1002/1873-3468.70435","DOIUrl":"https://doi.org/10.1002/1873-3468.70435","url":null,"abstract":"<p><p>Microbiome dysbiosis correlates with aging-associated pathological skin conditions, and our understanding of how the microbiome regulates skin aging at a molecular level is rapidly advancing. Classical hallmarks of skin aging, including genomic instability and telomere attrition, loss of proteostasis, epigenetic alterations, and altered intercellular communication, are critically regulated by the microbiome. Oxidative stress represents a key factor implicated in virtually all hallmarks of skin aging. Meanwhile, recent data underscore the role of metabolism in intercellular communication and aging. Here, we examine current evidence linking the skin microbiome to such molecular events in the aging skin.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148765384","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
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