Free Radical Research最新文献

{"title":"\"Therapeutic Potential of Nicotine in Modulating Oxidative and Mitochondrial Pathways in a C. elegans Parkinson's Disease Model\".","authors":"Inam Ullah, Shahab Uddin, Wang Xin, Hongyu Li","doi":"10.1080/10715762.2025.2567430","DOIUrl":"https://doi.org/10.1080/10715762.2025.2567430","url":null,"abstract":"<p><p>BackgroundParkinson's disease (PD) is one of the most widespread neurodegenerative diseases that affect the central nervous system (CNS) in elderly individuals. As of right now, there is no recognized cure for this illness. Parkinson's disease is not developing because of new medications. Bioactive phytochemicals are a natural alternative that can help older persons postpone age-related cognitive diseases.PurposeCurrently, FDA-licensed medicines for Parkinson's disease only provide symptomatic relief. This study attempts to establish whether nicotine, an alkaloid found naturally in nightshade plants, especially tobacco, may diminish parkinsonism in a model of Caenorhabditis elegans disease.MethodsThis study analyzes the antioxidant and restorative mitochondrial dysfunction potential of nicotine and its related neuroprotective benefits by utilizing models of Caenorhabditis worm strains that are different from the wild type. We examined the effects of nicotine on oxidative stress tolerance and associated regulatory pathways using a model of Caenorhabditis worms.ResultsOur results showed that wild-type C. elegans treated with nicotine had higher survival rates during oxidative stress caused by Juglone than those treated with the control. Nicotine decreased intracellular reactive oxygen species levels in C. elegans. In addition, nicotine increased levels of SOD, CAT, and MDA as well as the expression of genes related to stress response, including gst-4, hsf-6, and hsf-1, and mitochondrial function genes, including mev-1, isp-1, and cox-4. Finally, our molecular analysis indicates that the anti-oxidative effects of nicotine are mediated via skin-1 modulation. After Paraquat was administered, nicotine therapy also resulted in higher levels of ATP and MMP.ConclusionOur research clarifies the various mechanisms of action and communication pathways that underlie nicotine's antioxidant activity in vivo, offering a solid pharmacological foundation for its potential therapeutic use in neurodegeneration.</p>","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":" ","pages":"1-23"},"PeriodicalIF":2.9,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145191506","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}

{"title":"Betulinic acid protects sH-SY5Y cells exposed to lipopolysaccharide and ferrous sulfate through p38MAPK/NF-κB/GPX4/Nrf2/keap-1/HO-1 signaling axis.","authors":"Shivam Kumar Pandey, Hardev Singh, Shad Ahmad, Rakesh Kumar Singh","doi":"10.1080/10715762.2025.2565686","DOIUrl":"10.1080/10715762.2025.2565686","url":null,"abstract":"<p><p>Betulinic acid (BA) is a pentacyclic triterpenoid with broad pharmacological potential and widely recognized for its neuroprotective effects. This study investigated the potential protective effects of this compound on <i>in vitro</i> differentiated human neuroblastoma SH-SY5Y cells against LPS and FeSO₄-induced ferroptosis, apoptosis, neuroinflammation, and dopaminergic cell death, and explored the underlying mechanisms. Differentiated human neuroblastoma SH-SY5Y cells were exposed to LPS and FeSO₄, and the cellular viability was evaluated using the MTT assay. Flow cytometry was performed to assess apoptotic cell death. Additionally, the expression levels of key markers associated with ferroptosis, apoptosis, and other relevant signaling proteins were analyzed through western blotting and Immunocytochemical staining techniques. However, co<b>-</b>exposure with LPS and FeSO₄ resulted in a dose-dependent reduction in cell viability, which was significantly reversed by pretreatment with BA (0.3-30μM). Exposure to LPS and FeSO₄ increased the DMT1, Bax, caspase-3, and alpha-synuclein, and decreased the GPX4, FTH1, SLC7A11, Nrf2, Keap1, HO-1, PARK7, Bcl-2, NeuN, and TH levels, resulting in cell ferroptosis, apoptosis, and dopaminergic cell death. Furthermore, LPS and FeSO₄ significantly increased the expression of IL-6, TNF-α, and phosphorylation of p38, pMAPK, and pNFkB in the cells. Pretreatment with BA markedly suppressed LPS and FeSO₄-induced upregulation of pro-inflammatory cytokines, ferroptosis, apoptosis, and dopaminergic cell death markers. These findings suggest that BA exerts neuroprotection by modulating the GPX4/Nrf2/Keap-1/HO-1 antioxidant defense and p38MAPK/NF-κB inflammatory signaling pathways, highlighting its potential as a therapeutic agent for oxidative stress-related neurodegenerative conditions, such as Parkinson's disease (PD).</p>","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":" ","pages":"1-19"},"PeriodicalIF":2.9,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145124248","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}

{"title":"The interplay between microRNAs and oxidative stress and its implications in respiratory diseases.","authors":"Pushpendra Kumar Namdeo, Sehal Mishra, Amritha Das, Rajnarayan R Tiwari, Rajasekaran Subbiah","doi":"10.1080/10715762.2025.2564674","DOIUrl":"10.1080/10715762.2025.2564674","url":null,"abstract":"<p><p>MicroRNAs (miRNAs) (miRs) are a small class of endogenous non-coding RNA molecules that play a key role in various physiological and pathological processes. Likewise, oxidative stress can cause damage to many parts of the body and can contribute to disease development. Hence, this review aims to address the crosstalk between reactive oxygen species (ROS) and miRNAs in respiratory diseases. This review begins with an overview of the sources and regulation of free radicals, oxidative stress-mediated lung pathologies, and miRNAs biogenesis. Indeed, growing evidence suggests that miRNAs can modify cellular redox status in both nonmalignant and malignant respiratory diseases. We also discussed ROS-responsive miRNAs that have implications in disease development. Mechanistic pathways by which the complex interplay between miRNAs and ROS occurs have been discussed. Thus, targeting miRNAs may provide potential new strategies to specifically overcome oxidative stress-mediated development of many lung diseases.</p>","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":" ","pages":"1-21"},"PeriodicalIF":2.9,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145124165","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}

{"title":"Differential dihydroethidium fluorescence spectra in cell-free and cellular superoxide models: roles of riboflavin, FMN, FAD, and ions.","authors":"Bong-Geum Jang, Boyoung Choi, Ji-Eun Kim, Min-Ju Kim","doi":"10.1080/10715762.2025.2564671","DOIUrl":"10.1080/10715762.2025.2564671","url":null,"abstract":"<p><p>Dihydroethidium (DHE) is widely used for superoxide detection, yet reported excitation and emission values vary across studies. To address this, we employed full-spectrum scanning to compare DHE fluorescence between a xanthine oxidase (XO)-based cell-free system and a rotenone-treated cellular model, and to assess factors contributing to spectral shifts. In the XO system, the excitation peak was ∼480 nm, whereas in cells it shifted to ∼520 nm. Riboflavin, flavin mononucleotide (FMN), and flavin adenine dinucleotide (FAD) accounted for this shift, while calcium and bicarbonate ions modulated both peak position and fluorescence intensity. Riboflavin depletion reduced intracellular flavin levels but did not restore the peak to 480 nm, indicating additional roles for FMN and FAD. Among scavengers, only tiron directly inhibited DHE fluorescence in the cell-free system, with enhanced activity in the presence of Ca²⁺ and Mg²⁺. In contrast, responses in cells varied by type and rotenone concentration, suggesting indirect modulation through endogenous antioxidant defenses. Addition of FMN, FAD, or cell lysates to the cell-free system attenuated scavenger efficacy, supporting intracellular interference. These findings demonstrate that riboflavin metabolism and ionic microenvironments critically shape DHE spectral behavior. Accurate interpretation of DHE-based superoxide detection therefore requires prior spectral evaluation to distinguish genuine superoxide signals from cofactor- or ion-dependent effects.</p>","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":" ","pages":"1-21"},"PeriodicalIF":2.9,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145112113","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}

{"title":"Copper induces cystine/glutamate antiporter SLC7A11 through the activation of Nrf2 and Atox1 pathways.","authors":"Tetsuro Kamiya, Ryoka Teruya, Haruka Tahara, Yuki Inoue, Aoi Ikeda, Sayaka Hosowari, Tomo Arioka, Tomohiro Otsuka, Hirokazu Hara","doi":"10.1080/10715762.2025.2560847","DOIUrl":"10.1080/10715762.2025.2560847","url":null,"abstract":"<p><p>Amino acid metabolism plays a crucial role in tumor biology. The sodium-independent cystine/glutamate exchange system, known as system X_c^-, is significantly activated in cancer cells and plays a role in tumor progression. Copper (Cu), an essential micronutrient, plays a crucial role in physiological processes; however, its accumulation in tumors has been associated with tumor progression. Nonetheless, the relationship between system X_c^--mediated amino acid metabolism and Cu remains inadequately understood. In this study, CuCl₂ treatment resulted in the significant induction of SLC7A11, a light chain subunit of system X_c^-, and glutamate receptor mGluR1 expression in human triple-negative MDA-MB-231 cells. Conversely, FeCl₂ treatment induced the expression of SLC7A11 but not mGluR1, indicating that Cu specifically activated SLC7A11-mediated amino acid metabolism. The investigation focused on the role of Nrf2, a redox-sensitive transcription factor, in the induction of SLC7A11 under conditions of oxidative stress induced by CuCl₂ treatment. Upon treatment with CuCl₂, the nuclear translocation of Nrf2 was observed, and knockdown of Nrf2 significantly suppressed the induction of SLC7A11. Given that the Cu chaperone, antioxidant-1 (Atox1), functions as a Cu-dependent transcription factor, the role of Atox1 in the expression of SLC7A11 was further investigated. Like the effects of Nrf2 knockdown, Atox1 was found to play a pivotal role in the Cu-mediated induction of SLC7A11. Our findings indicate that intratumoral Cu influences the expression of SLC7A11 and may play a role in tumor progression.</p>","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":" ","pages":"1-12"},"PeriodicalIF":2.9,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145052751","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}

{"title":"Selenoprotein GPX3 suppresses gastric adenocarcinoma proliferation and improves patient survival.","authors":"Chunfeng Zhang, Lijuan Ma, Ying Shao, Shanpeng Cui, Li Li","doi":"10.1080/10715762.2025.2551031","DOIUrl":"https://doi.org/10.1080/10715762.2025.2551031","url":null,"abstract":"<p><p>Stomach adenocarcinoma (STAD) is a highly prevalent and lethal malignancy worldwide, with its occurrence and progression regulated by multiple factors. In recent years, selenoprotein glutathione peroxidase 3 (GPX3) has gained significant attention due to its antioxidant properties and role in cellular oxidative stress regulation across various cancers. Our study delved into the expression of GPX3 in STAD and investigated its impact on tumor cell growth, providing insights into its potential anti-tumor mechanisms. The expression levels of GPX3 were analyzed in STAD tissues sourced from the TCGA database and contrasted with the levels found in normal gastric tissues. The expression levels of GPX3 were contrasted between STAD tissues and normal gastric tissues, and their correlation with patient prognosis was assessed by survival analysis. Additionally, we validated GPX3 expression changes and its effects on tumor cell growth using quantitative PCR (qPCR) and CCK-8 proliferation assays in STAD cell lines (MNK-45, MGC-803, N87, and HGC-27). Our findings suggest that GPX3 expression is significantly downregulated in STAD tissues compared to normal gastric tissues. Survival analysis further reveals that patients with high GPX3 expression exhibit better long-term survival rates, suggesting a potential tumor-suppressive function. <i>In vitro</i> experiments confirmed effective knockdown or overexpression of GPX3 in STAD cell lines. CCK-8 proliferation assays demonstrated that GPX3 overexpression significantly inhibited tumor cell proliferation, whereas GPX3 knockdown promoted cell growth. This study provides new experimental evidence supporting GPX3 as a potential therapeutic target for STAD and offers a theoretical foundation for future molecular-targeted therapies for STAD.</p>","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":" ","pages":"1-9"},"PeriodicalIF":2.9,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144948652","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}

{"title":"Pseudohypoxia induced by iron chelator activates tumor immune response in lung cancer.","authors":"Yusuke Hamada, Toshiaki Ohara, Yuehua Chen, Manato Terada, Yuze Wang, Hotaka Kawai, Masayoshi Fujisawa, Teizo Yoshimura, Akihiro Matsukawa","doi":"10.1080/10715762.2025.2551030","DOIUrl":"https://doi.org/10.1080/10715762.2025.2551030","url":null,"abstract":"<p><p>Hypoxia-inducible factor (HIF) signaling plays a critical role in immune cell function. Pseudohypoxia is characterized as iron-mediated stabilization of HIF-1α under normoxic conditions, which can be induced by iron chelators. This study explored whether iron chelators exert antitumor effects by enhancing tumor immune responses and elucidating the underlying mechanisms. The iron chelators Super-polyphenol 10 (SP10) and Deferoxamine (DFO) were used to create iron-deficient and pseudohypoxia conditions. Pseudohypoxia induced by iron chelators stimulates IL-2 secretion from T cells and from both human and murine nonsmall cell lung cancer (NSCLC) cell lines (A549, PC-3, and LLC). Administration of SP10 reduced tumor growth when LLC tumors were implanted in C57BL/6 mice; however, this was not observed in immunodeficient RAG1-deficient C57BL/6 mice. SP10 itself did not directly inhibit LLC cells proliferation <i>in vitro</i>, suggesting an activation of the tumor immune response. SP10 synergistically enhanced the efficacy of PD-1 antibody therapy in lung cancer by increasing the number of tumor-infiltrating lymphocytes (TILs). In conclusion, iron chelation-induced pseudohypoxia activates tumor immune responses by directly upregulating HIF-1α, augmenting T cell function, and inducing IL-2 secretion from T cells, and cancer cells, thereby amplifying the immune efficacy of the PD-1 antibody in lung cancer treatment.</p>","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":" ","pages":"1-13"},"PeriodicalIF":2.9,"publicationDate":"2025-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144948637","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}

{"title":"Far-infrared radiation-mediated GPx-1/eNOS/ERK signaling contributes to the protective potential against methamphetamine-caused impairments in recognition memory in mice.","authors":"Eun-Joo Shin, Yoon Hee Chung, Bao Trong Nguyen, Naveen Sharma, Ngoc Kim Cuong Tran, Yen Nhi Doan Nguyen, Jung Hoon Park, Dae-Joong Kim, Toshitaka Nabeshima, Ji Hoon Jeong, Hyoung-Chun Kim","doi":"10.1080/10715762.2025.2551032","DOIUrl":"https://doi.org/10.1080/10715762.2025.2551032","url":null,"abstract":"<p><p>Far-infrared radiation (FIR) induces glutathione peroxidase-1 (GPx-1) expression and enhances microcirculation by upregulating endothelial nitric oxide synthase (eNOS). However, the role of eNOS in FIR-mediated neuroprotection remains unclear. Here, we investigated whether FIR upregulates eNOS and extracellular signal-regulated kinase (ERK) signaling to mitigate recognition memory impairment caused by methamphetamine (MA). FIR significantly reduced MA-induced oxidative stress, which was primarily associated with GPx-1 inhibition. FIR or genetic overexpression of GPx-1 (GPx-1 TG) in mice significantly attenuated the MA-induced reduction in phospho-eNOS (p-eNOS) and phospho-ERK (p-ERK). Triple-label immunostaining revealed colocalization of p-eNOS, p-ERK, and GPx-1 within the same cellular populations in the prefrontal cortex. In non-transgenic (non-TG) mice, FIR exposure improved MA-induced cholinergic and memory deficits. However, FIR did not provide additional cognitive benefits in GPx-1 TG mice, and the GPx-1 inhibitor mercaptosuccinate blocked FIR-mediated cholinergic effects. Inhibitors of eNOS (i.e. L-NAME) and ERK (i.e. U0126) also significantly blocked the FIR-driven memory-enhancing effects in non-TG mice. Unlike L-NAME, which inhibits phosphorylation of both eNOS and ERK, U0126 did not affect FIR-induced eNOS phosphorylation, suggesting that eNOS is an upstream molecule for ERK signaling. Our finding suggests that GPx-1 is an essential mediator of FIR-induced memory enhancement, and that FIR exposure attenuates MA-induced cognitive impairments <i>via</i> cholinergic upregulation associated with GPx-1/eNOS/ERK signaling.</p>","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":" ","pages":"1-25"},"PeriodicalIF":2.9,"publicationDate":"2025-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144948613","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}

{"title":"Unveiling the Anti-aging Activities and Mechanism of Melibiose: Insights from Metabolomics and RT-qPCR Analyses.","authors":"Xu Chen, Jiazheng Liang, Tianyu Zheng, Zhijun Su, Shaojun Yu, Han Yu, Bo Wang, Yuanyuan Zhang, Yonggang Liu","doi":"10.1080/10715762.2025.2551848","DOIUrl":"https://doi.org/10.1080/10715762.2025.2551848","url":null,"abstract":"<p><p>In this study, the anti-aging potential of melibiose was examined, and its molecular mechanism was elucidated using <i>Caenorhabditis elegans</i> as a model organism. The findings demonstrated that melibiose at concentrations of 100 μM, 150 μM, and 200 μM significantly increased nematode lifespan by 15.38%, 23.08%, and 30.77% respectively. Additionally, melibiose enhanced resistance against heat and oxidative stress, improved nematode motility, reduced lipofuscin and reactive oxygen species (ROS) accumulation, and increased antioxidant enzyme activity. Through the use of gene-deletion nematodes, transgenic nematodes, RT-qPCR, and metabolomics, it was determined that melibiose potentially exerts its effects through multiple pathways including the insulin signaling pathway (down-regulation of <i>daf-2</i> and <i>age-1</i>, up-regulation of <i>sod-3</i> and <i>hsp-16.2</i>), the AMP-activated protein kinase (AMPK) pathway (up-regulation of <i>aak-2</i>), and the JNK pathway (up-regulation of <i>jnk-1</i>). Activation of transcription factors DAF-16, SKN-1, and HSF-1 was observed, moreover, delaying the aging process by promoting autophagy (upregulation of <i>lgg-1</i> and <i>bec-1</i>) and mitochondrial function (upregulation of <i>hsp-6</i>, <i>hsp-60</i>, and mev-1) to resist oxidative damage. And its anti-aging signature metabolites may be Carbimazole, 4-Hydroxy-2-oxoglutaric acid, and 1,4-Dithiothreitol.</p>","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":" ","pages":"1-17"},"PeriodicalIF":2.9,"publicationDate":"2025-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144948609","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}

{"title":"Mitochondria and redox homeostasis - the backseat drivers in glioma.","authors":"Shruti Patrick, Ellora Sen","doi":"10.1080/10715762.2025.2548479","DOIUrl":"10.1080/10715762.2025.2548479","url":null,"abstract":"<p><p>Mitochondrial function and redox regulatory processes are crucial aspects of cellular metabolism and energy production. Cancers, including gliomas, largely exhibit altered mitochondrial function, which can lead to changes in cellular signaling pathways and redox homeostasis. Aberrant redox signaling can promote glioma progression by influencing cell proliferation, metastasis, and therapeutic response. Several cancer-associated driver mutations - genetic alterations that confer survival and growth advantage to cancer cells, are associated with gliomas and affect mitochondrial function and redox states. Here is an overview of the crucial intersection between mitochondrial function and driver genes in glioma, highlighting some of the recent advances that augment our understanding of this intersection.</p>","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":" ","pages":"1-13"},"PeriodicalIF":2.9,"publicationDate":"2025-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144845317","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}