Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe最新文献

{"title":"Advancements in mitochondrial-targeted antioxidants: Organelle-specific drug delivery for disease management","authors":"Nazmun Nahar ,&nbsp;Md. Shihab Uddin Sohag","doi":"10.1016/j.arres.2025.100142","DOIUrl":"10.1016/j.arres.2025.100142","url":null,"abstract":"<div><div>Mitochondria, a crucial subcellular organelle, serve as the primary generator of reactive oxygen species (producing around 90 % of total ROS), utilizing over 98 % of cellular oxygen for ATP synthesis while converting 1–2 % into ROS. Excess reactive oxygen species disrupt redox homeostasis, inducing oxidative stress, resulting in mitochondrial dysfunction and damage. Furthermore, defective or impaired mitochondria might intensify ROS production. This \"necessary evil\" serves dual functions: regulating signaling, apoptosis, proliferation, differentiation, autophagy, and immunological responses while simultaneously inflicting oxidative damage on lipids, proteins, and DNA, hence contributing to numerous diseases. Thus, the targeted suppression of mitochondrial ROS-induced oxidative damage and dysfunction by mitochondria-targeted antioxidants (MTAs) represents a precise therapeutic strategy that has attracted growing interest and offers substantial opportunities for clinical application by directly alleviating oxidative stress at its origin within affected cells. Lipophilic cation-linked MTAs, amino acid- and peptide-based MTAs, metallo-complex-based MTAs, and nanoparticle-based MTAs (Nano-MTAs) can selectively localize to mitochondria and diminish excessive mitochondrial ROS. Incorporating these MTAs into precision medicine facilitates tailored therapies based on individual mitochondrial dysfunction characteristics and disease-specific redox imbalances. This review classifies current mitochondria-targeted antioxidants according to the characteristics of their targeting moieties and examines their composition and antioxidant efficacy. We also evaluate nanoparticle-based MTAs, including liposomes, DQAsomes, solid lipid nanoparticles, MITO-Porters, micelles, dendrimers, nanoemulsions, metal nanoparticles, quantum dots, and nanopolyplexes. Furthermore, we summarize recent experimental findings regarding MTAs across diverse disease models including cancer, neurological disorders (e.g., Alzheimer’s, Huntington’s, Parkinson’s, ataxia, TBI, and epilepsy); cardiovascular diseases; asthma; COPD; auditory impairments; diabetic complications; ocular, renal, hepatic, and inflammatory disorders; sepsis; infertility; aging-longevity; and their potential as antibiotics to clarify the evidence supporting their therapeutic efficacy.</div></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"17 ","pages":"Article 100142"},"PeriodicalIF":2.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145624035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mapping transcriptomic signatures downstream of mitochondrial superoxide dismutase SOD2 in OVCA433 multicellular aggregates","authors":"Amal Taher Elhaw ,&nbsp;Priscilla W. Tang ,&nbsp;Shriya Kamlapurkar ,&nbsp;Sarah Al-Saad ,&nbsp;Sneha Srinivasan ,&nbsp;Danyang Li ,&nbsp;George C. Tseng ,&nbsp;Adam C. Straub ,&nbsp;Nadine Hempel","doi":"10.1016/j.arres.2025.100141","DOIUrl":"10.1016/j.arres.2025.100141","url":null,"abstract":"<div><div>During metastatic spread, tumor cells adapt to evade anchorage-independent cell death by upregulating mitochondrial antioxidant systems. We previously showed that ovarian cancer cells upregulate mitochondrial manganese superoxide dismutase (SOD2) following detachment and multicellular aggregate (MCA) formation. SOD2 scavenges mitochondrial superoxide and manipulates cellular hydrogen peroxide levels, both functions necessary for metastasis. Here, we investigated SOD2′s metastatic function by assessing its transcriptomic effects in OVCA433 ovarian cancer cells cultured in low-attachment conditions that induce MCAs, mimicking anchorage-independent states in malignant ascites. SOD2 siRNA-mediated knockdown effects in MCAs were compared to adherent culture conditions. RNA sequencing and pathway analysis revealed that SOD2 lies upstream of pro-metastatic pathways, including PI3K/AKT signaling. Notably, in MCAs, cytokine and immune cell signaling pathways were more significantly enriched following SOD2 knockdown. We previously identified SIRT3 as an important SOD2 activity regulator in MCAs. While SIRT3 knockdown resulted in minor transcriptional changes, we identified that FOXO3 and ELF4 transcription factors, important for stress response and immune regulation, are downregulated by both SIRT3 and SOD2 knockdown. Comparing SOD2 knockdown transcriptional changes to the Cancer Genome Atlas, we found SOD2 expression strongly associates with pro-tumorigenic immune signaling in serous ovarian cancer specimens, including genes identified downstream of SOD2 from our siRNA screen. Moreover, SOD2 expression correlated with signatures related to pro-tumorigenic neutrophil and T-regulatory cell populations. Our data suggest SOD2 positively regulates pro-metastatic pathways, and those identified in MCAs more closely reflect gene expression profiles associated with SOD2 expression in patient tumors.</div></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"17 ","pages":"Article 100141"},"PeriodicalIF":2.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145528713","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oxidative stress-induced cytotoxicity and the role of dietary antioxidants in farm animals: A review","authors":"Muhammad Khan ,&nbsp;Maida Mushtaq ,&nbsp;Muhammad Usman ,&nbsp;Muhammad Aziz Ur Rahman ,&nbsp;Guobo Quan","doi":"10.1016/j.arres.2025.100138","DOIUrl":"10.1016/j.arres.2025.100138","url":null,"abstract":"<div><div>Oxidative stress, resulting from an imbalance between reactive oxygen species (ROS) and antioxidant defenses, impairs animal health, immunity, reproduction, and productivity. This review summarizes the roles of key dietary antioxidants vitamin A, melatonin, essential trace minerals (copper, zinc, magnesium), flavonoids, polyphenols, and L-carnitine, in mitigating oxidative stress in farm animals. Vitamin A supports epithelial integrity, scavenges ROS, and upregulates antioxidant enzymes via redox-sensitive transcription factors. Melatonin functions as a potent free radical scavenger and activates the Nrf2 pathway to enhance antioxidant enzyme expression. Copper, zinc, and magnesium act as cofactors for enzymatic antioxidants such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), helping maintain redox homeostasis. Flavonoids and polyphenols, including quercetin, curcumin, and EGCG, exert antioxidant effects by scavenging ROS, chelating metal ions, and enhancing endogenous defense pathways. L-carnitine improves mitochondrial function, reduces ROS generation, and enhances glutathione activity, especially during stress conditions such as heat, transport, or weaning. Supplementation with these compounds across species has been shown to increase antioxidant enzyme activity, reduce oxidative biomarkers like malondialdehyde (MDA), and improve immunity, metabolic efficiency, and performance. These natural or synthetic antioxidants offer promising nutritional strategies to improve oxidative stability, health, and productivity in farm animals. Their integration into feed programs provides a sustainable and cost-effective approach to improving animal welfare and resilience under intensive production systems.</div></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"16 ","pages":"Article 100138"},"PeriodicalIF":2.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144748957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Altered activity of leukocytes derived from circulating blood immediately after revascularization in peripheral artery disease","authors":"Kozo Takeuchi ,&nbsp;Kimiko Kazumura ,&nbsp;Akihiro Yoshida ,&nbsp;Tappei Furuta ,&nbsp;Kazunori Hayashi ,&nbsp;Masashi Nagai ,&nbsp;Yukiko Hatano ,&nbsp;Michitaka Naito ,&nbsp;Etsushi Matsushita","doi":"10.1016/j.arres.2025.100137","DOIUrl":"10.1016/j.arres.2025.100137","url":null,"abstract":"<div><div>Endovascular treatment (EVT) is an effective therapeutic option for patients with peripheral artery disease (PAD). However, EVT is associated with inflammatory adverse effects, and the systemic oxidative status after EVT remains unclear. In this pilot study, we compared the activity of leukocytes derived from circulating blood before and immediately after (within 1 h of) EVT in 30 cases with PAD. The ankle-brachial index (ABI) improved immediately after EVT (<em>p</em> &lt; 0.001), suggesting successful revascularization. The levels of leukocyte-produced superoxide radicals (O₂^•−) increased (<em>p</em> &lt; 0.05), those of hypochlorite ions (OCl⁻) remained unchanged, and the OCl⁻/O₂^•− levels reduced (<em>p</em> &lt; 0.001) immediately after EVT. We observed two subtypes of alterations in leukocyte activity immediately after EVT: type A exhibiting increased levels of both O₂^•− and OCl⁻, and type B showing increased O₂^•− levels, while relatively small changes in OCl⁻ levels. In addition, the interleukin-6 levels increased (<em>p</em> &lt; 0.05) immediately after EVT. Moreover, EVT increased the leukocyte count (<em>p</em> &lt; 0.001) and dynamically changed the balance of leukocyte components, with a notable increase in the neutrophil percentage. These findings and results of our correlation analyses imply that inflammatory response and/or ischemia–reperfusion potentially alters O₂^•−production by leukocytes. This study contributes to the understanding of the pathophysiology of EVT-associated systemic oxidative events, which includes vascular inflammation and ischemia–reperfusion injury. The findings can support further development of diagnostic and therapeutic strategies for the health conditions after EVT.</div></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"16 ","pages":"Article 100137"},"PeriodicalIF":0.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144534320","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Redox signalling and microRNA feedback in exercise-mediated skeletal muscle remodelling","authors":"Qin Xia ,&nbsp;Katarzyna Goljanek-Whysall ,&nbsp;Brian McDonagh","doi":"10.1016/j.arres.2025.100133","DOIUrl":"10.1016/j.arres.2025.100133","url":null,"abstract":"<div><div>Exercise induces the acute generation of reactive oxygen species (ROS) in skeletal muscle, which can regulate a range of redox signalling pathways that determine the adaptive response to exercise. The redox environment can directly affect excitation contraction coupling, calcium handling and inflammation but also regulate key signalling pathways involved in mitochondrial quality control and proteostasis. Additionally, exercise-induced regulation of microRNAs (miRs) levels can provide a feedback mechanism to fine tune the adaptive response. Endogenous ROS produced during exercise arise from diverse sources including NADPH oxidases (NOX), mitochondria, xanthine oxidase (XO) and phospholipase A2 (PLA2). As high levels of ROS can potentially be damaging, there is a sophisticated, organelle-specific antioxidant network in skeletal muscle that includes superoxide dismutases (SODs), catalases (CATs), peroxiredoxins (PRDXs) and glutathione peroxidases (GPXs). Due to their abundance, location and catalytic activity, emerging evidence highlights the potential role of the PRDX family as central mediators in coordinating the redox signalling cascade as a result of increased ROS generation. Several exercise related miRs contain binding sites for redox sensitive and exercise associated transcription factors (TFs), moreover some miRs can target these TFs, providing a potential feedback mechanism to maintain cellular homeostasis following disruption of the redox environment. The interconnected roles of redox signalling and miRs are discussed in exercise-induced skeletal muscle adaptations. Furthermore, the therapeutic potential of targeting these interconnected pathways to mitigate muscle ageing and dysfunction, can provide valuable insights into strategies for optimising muscle health and enhancing healthspan.</div></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"16 ","pages":"Article 100133"},"PeriodicalIF":0.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144196228","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of cell culture conditions on NRF2 (nuclear factor E2 p45-related factor 2)-driven reporter gene expression","authors":"Barbara Braunböck-Müller,&nbsp;Elke H Heiss","doi":"10.1016/j.arres.2025.100136","DOIUrl":"10.1016/j.arres.2025.100136","url":null,"abstract":"<div><div>For the identification and characterization of compounds that modulate the activation status of the stress-responsive and cytoprotective transcription factor NRF2 (nuclear factor E2 p45-related factor 2), ARE (antioxidant response element)-driven reporter gene assays serve as convenient tools. NRF2 signaling is susceptible to various factors, including cellular energy status, circadian rhythm, and mechanical or oxygen tension. These parameters are often inadequately accounted for in routine 2D cell culture and screening processes, potentially limiting the relevance of the obtained data or identified hits. Therefore, we investigated whether NRF2-driven luminescence readings from a ARE-luciferase reporter gene markedly differ from routine culture conditions when stably transfected HepG2 cells are cultivated in plasma-like medium, exhibit altered mechanotransduction, are synchronized, or grown in spheroids. While NRF2 signaling is consistently activated by the synthetic triterpenoid CDDO-IM under all tested conditions, the baseline (indicative for the initial cellular stress status/Nrf2 activity) and/or the extent of inducible luciferase activity (activation amplitude conferred by the NRF2 activator) varies across different cultivation conditions.</div></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"16 ","pages":"Article 100136"},"PeriodicalIF":0.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144263840","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of abnormal mitochondrial DNA in Cancer: A review of molecular changes and therapeutic opportunities","authors":"Md. Sanower Hossain ,&nbsp;Mohammad Touhidul Islam ,&nbsp;Md. Abid Hossain ,&nbsp;Kajima Rifat ,&nbsp;Saila Kabir Maeesa ,&nbsp;Mamunur Rahman ,&nbsp;Md. Rezaul Islam ,&nbsp;Raihana Edros ,&nbsp;Sheikh Zahir Raihan ,&nbsp;Chrismawan Ardianto ,&nbsp;Long Chiau Ming ,&nbsp;Bey Hing Goh ,&nbsp;Mohd Yusri Bin Mohd Yunus ,&nbsp;Jun Haslinda Shariffuddin","doi":"10.1016/j.arres.2025.100134","DOIUrl":"10.1016/j.arres.2025.100134","url":null,"abstract":"<div><div>Mitochondria are cellular organelles that play vital roles in a cell's energy production and metabolism. Researchers have made significant progress in understanding mitochondrial dynamics and their effects on human health in recent years. The mitochondrial genome or respiratory chain induces mitochondrial illnesses. Mitochondrial DNA (mtDNA) is a crucial component of mitochondria, and its relationship with cancer has received much attention in recent years. Although there is currently no cure for mitochondrial disorders, various treatment options, such as physiotherapy, hearing aids, pacemakers, and sodium bicarbonate injections, are available for managing symptoms. Diet and exercise can help patients with mitochondrial dysfunction. Individuals with pyruvate dehydrogenase insufficiency benefit from a ketogenic diet and a high-fat, low-carbohydrate diet. Cancer is linked to mitochondrial dynamics, including fusion and fission. These pathways affect cancer stem cell proliferation and recurrence. New cancer therapies may be developed by targeting the proteins involved in mitochondrial fusion and fission. Although some trials have already been conducted, additional research is needed to establish this phenomenon as a full treatment option.</div></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"16 ","pages":"Article 100134"},"PeriodicalIF":0.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144595693","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deciphering of the reactive oxygen species (ROS) induced calpain activation in cancer progression and its therapeutic potential","authors":"Krishna Samanta ,&nbsp;Ivan Ahel ,&nbsp;Pulak Kar","doi":"10.1016/j.arres.2025.100124","DOIUrl":"10.1016/j.arres.2025.100124","url":null,"abstract":"<div><div>Mitochondrial signalling plays a fundamental role in orchestrating essential intracellular functions, including cellular respiration, proliferation, nucleic acid synthesis, and oxidative stress management. The activation of calpain, a group of Ca²⁺-dependent cysteine proteases, by ROS-induced oxidative stress is linked to cancer progression. Calpain can be activated by ROS either through intracellular Ca²⁺ elevation or via oxidative modifications of the protease, altering protein susceptibility to calpain cleavage. In tumour cell biology, ROS-activated calpains influence cell survival, migration, proliferation, apoptosis, and invasiveness. Several studies report unusual calpain expression in cancer cells. Various anticancer drugs induce cytotoxicity by activating calpain, significantly impacting cancer treatment strategies. This unique review explores the perspective of ROS-induced calpain activation and its pivotal role in cancer progression and therapeutics.</div></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"15 ","pages":"Article 100124"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143577739","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exogenously added recombinant CLIC proteins provide antioxidant protection to cells in culture","authors":"KR Hossain,&nbsp;A Alghalayini,&nbsp;DR Turkewitz,&nbsp;C D’Amario,&nbsp;Catherine A Gorrie,&nbsp;M Wallach,&nbsp;SM Valenzuela","doi":"10.1016/j.arres.2025.100132","DOIUrl":"10.1016/j.arres.2025.100132","url":null,"abstract":"<div><div>Chloride intracellular ion channels (CLICs) are a family of six human proteins that exist as both soluble and integral membrane proteins and are expressed across a range of different tissues throughout the body. CLIC1 and CLIC4 act as moonlighting proteins, exhibiting oxidoreductase enzymatic activity in addition to their membrane ion channel activity. Transient siRNA knockdown of either CLIC1 or CLIC4 in primary human dermal fibroblast (HDF), human epidermal keratinocyte (HKE) cells and in the stable murine fibroblast cell line, NIH/3T3, showed significant reduction in cell viability. Conversely, NIH/3T3 cells over-expressing CLIC1 or CLIC4 demonstrated that both proteins assist in protecting the cells from hydrogen peroxide (H₂O₂)-induced oxidative damage, resulting in reduced cell death and reduced Reactive Oxygen Species (ROS) generation. While the opposite effect was seen in cells where these proteins had been silenced using siRNA. We have also now demonstrated that by exogenously adding recombinant CLIC (rCLIC) proteins to either HDF or HKE cells in culture, both rCLIC1 and rCLIC4 proteins provided cellular antioxidant protection to the fibroblast and keratinocyte cells against H₂O₂-induced oxidative damage. Our study also demonstrates rCLIC1 and rCLIC4’s ability to act as skin cell protective antioxidant agents, arises from their oxidoreductase enzymatic activity. Our findings also showed exogenous addition of rCLIC1 or rCLIC4 to skin cells resulted in similar or greater protection against H₂O₂-induced oxidative damage when compared to other well-known endogenous antioxidants like glutaredoxin (Grx), Glutathione S-transferase-Omega (GST-Ω) and the antioxidant drug, N-acetylcysteine (NAC).</div></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"15 ","pages":"Article 100132"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144098738","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Global hotspots and prospective trends for chondrocyte metabolic changes and oxidative stress in osteoarthritis: A bibliometric analysis","authors":"Wuyan Lu ,&nbsp;Jieshen Huang ,&nbsp;Zhonglin Zhang ,&nbsp;Shuangmeng Jia ,&nbsp;Weiqiao Zhao ,&nbsp;Linxiao Li ,&nbsp;Fengting Niu ,&nbsp;Ke Fang ,&nbsp;Zixin Cai ,&nbsp;Yao Li ,&nbsp;Yishu Lu ,&nbsp;Lei Cui ,&nbsp;Jiefeng Huang ,&nbsp;Shuaijun Li","doi":"10.1016/j.arres.2025.100130","DOIUrl":"10.1016/j.arres.2025.100130","url":null,"abstract":"<div><div>Osteoarthritis (OA) is a prevalent age-related degenerative joint disorder characterized by dysregulation of metabolism. While several studies have examined the metabolic changes in OA, there exists a lack of a comprehensive retrospective analysis of its current development, research hotspots, and future trends. In this study, we employed bibliometric approaches to retrospectively review the development, mechanisms, and future trends of metabolic changes in OA. We utilized VOSviewer software to quantitatively and visually depict: (a) annual temporal trends in literature and citation counts; (b) national/regional publications and collaborations; (c) institutional and author contributions; (d) journal contributions and relevance; (e) analysis of research hotspots and directions through keywords. By analyzing keywords and research hotspots, we systematically illustrated the influential factors of metabolic changes in OA, including inflammation, apoptosis, oxidative stress, and autophagy. Conclusively, the research field of metabolic changes in OA is rapidly expanding, and we aim to provide a more comprehensive and insightful perspective for targeting metabolic disorders in OA.</div></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"15 ","pages":"Article 100130"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143799815","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}