Free Radical Biology and Medicine最新文献_第3页

Role of ferroptosis in mitochondrial damage in diabetic retinopathy 铁蛋白沉积在糖尿病视网膜病变线粒体损伤中的作用。

IF 7.1 2区生物学

Free Radical Biology and Medicine Pub Date : 2024-10-19 DOI: 10.1016/j.freeradbiomed.2024.10.296

{"title":"Role of ferroptosis in mitochondrial damage in diabetic retinopathy","authors":"","doi":"10.1016/j.freeradbiomed.2024.10.296","DOIUrl":"10.1016/j.freeradbiomed.2024.10.296","url":null,"abstract":"<div><div>Diabetic retinopathy is driven by oxidative stress-mitochondrial damage. Activation of ROS producing cytosolic NADPH oxidase 2 (Nox2) in diabetes precedes retinal mitochondrial damage, initiating a vicious cycle of free radicals. Elevated ROS levels peroxidize membrane lipids increasing damaging lipid peroxides (LPOs). While glutathione peroxidase 4 (GPx4) neutralizes LPOs, an imbalance in its generation-neutralization leads to ferroptosis, which is characterized by increased LPOs, free iron and decreased GPx4 activity. Mitochondria are rich in polyunsaturated fatty acids and iron and have mitochondrial isoform of GPx4. Our aim was to investigate mitochondrial ferroptosis in diabetic retinopathy, focusing on Nox2 mediated ROS production. Using human retinal endothelial cells, incubated in 5 mM or 20 mM D-glucose for 12–96 h, with or without Nox2 inhibitors (100 μM apocynin, 5 μM EHop-016 or 5 μM Gp91 ds-tat), or ferroptosis inhibitors (1 μM ferrostatin-1, 50 μM deferoxamine) or activator (0.1 μM RSL3), cytosolic and mitochondrial ROS, LPOs, iron, GPx4 activity, mitochondrial integrity (membrane permeability, oxygen consumption rate, mtDNA copy numbers) and cell death were quantified. High glucose significantly increased ROS, LPOs and iron levels and inhibited GPx4 activity in cytosol, and while Nox2 and ferroptosis inhibitors prevented glucose-induced increase in ferroptosis markers, mitochondrial damage and cell death, RSL3, further worsened them. Furthermore, high glucose also increased ferroptosis markers in the mitochondria, which followed their increase in the cytosol, suggesting a role of cytosolic ROS in mitochondrial ferroptosis. Thus, targeting Nox2-ferroptosis should help break down the self-perpetuating vicious cycle of free radicals, initiated by the damaged mitochondria, and could provide novel therapeutics to prevent/retard the development of diabetic retinopathy.</div></div>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":null,"pages":null},"PeriodicalIF":7.1,"publicationDate":"2024-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142461741","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Bioavailability of mango (poly)phenols: An evaluation of the impact of the colon, and phenylalanine and tyrosine on the production of phenolic catabolites 芒果（多）酚的生物利用率：评估结肠、苯丙氨酸和酪氨酸对产生酚类代谢产物的影响。

IF 7.1 2区生物学

Free Radical Biology and Medicine Pub Date : 2024-10-18 DOI: 10.1016/j.freeradbiomed.2024.10.289

{"title":"Bioavailability of mango (poly)phenols: An evaluation of the impact of the colon, and phenylalanine and tyrosine on the production of phenolic catabolites","authors":"","doi":"10.1016/j.freeradbiomed.2024.10.289","DOIUrl":"10.1016/j.freeradbiomed.2024.10.289","url":null,"abstract":"<div><div>A mango pulp purée was ingested by ileostomists, whose colon had been removed surgically, and subjects with a full gastrointestinal (GI) tract, after which ileal fluid, urine and feces were collected over a 24 h period and analysed by UHPLC-HR-MS. The main (poly)phenols in the purée were gallotannins (356 μmol) and two hydroxy-methoxy-cinnamoyl glucose esters (43 μmol) together with the aromatic amino acids phenylalanine (22 μmol) and tyrosine (209 μmol). Analysis of ileal fluid revealed almost all the ingested gallotannins appeared to have broken down in the upper GI tract with the released benzoic acids being rapidly absorbed into the circulatory system prior to urinary excretion mainly as phase-2 metabolites. Likewise, the glucose moiety of the cinnamic acid conjugates was cleaved and the released cinnamic acids absorbed efficiently from the proximal GI tract and subjected to phase II metabolism prior to excretion. Among the main phenolics excreted after mango intake were phenylacetic and benzoic acids and hydroxybenzene catabolites which were present in lower, but none-the-less, substantial amounts, in the urine of ileostomists. This indicates that a portion of these phenolics, including the hydroxybenzene derivatives, originate from substrates absorbed in the upper GI tract and are principally products of endogenous metabolism rather than being derived from colonic microbiota-mediated catabolism. 1,2,3-Trihydroxybenzene (aka pyrogallol) was the dominant urinary catabolite in both groups. Hippuric acid excretion exceeded (poly)phenol intake indicating a significant contribution from phenylalanine and tyrosine. The aromatic amino acids, while present in the ingested pulp, can also originate from several sources including breakdown of dietary proteins in the GI tract, and endogenous breakdown of surplus mammalian proteins independent of the GI tract. The trial was registered at clinical <span><span>trials.gov</span><svg><path></path></svg></span> as NCT06182540.</div></div>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":null,"pages":null},"PeriodicalIF":7.1,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142461830","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Mitochondrial malfunction-initiated Leydig cell premature senescence partially participates in 1-nitropyrene-evoked downregulation of steroidogenic synthases in testes 线粒体功能失调引发的亮德细胞早衰部分参与了 1-硝基芘诱发的睾丸类固醇合成酶下调。

IF 7.1 2区生物学

Free Radical Biology and Medicine Pub Date : 2024-10-18 DOI: 10.1016/j.freeradbiomed.2024.10.291

{"title":"Mitochondrial malfunction-initiated Leydig cell premature senescence partially participates in 1-nitropyrene-evoked downregulation of steroidogenic synthases in testes","authors":"","doi":"10.1016/j.freeradbiomed.2024.10.291","DOIUrl":"10.1016/j.freeradbiomed.2024.10.291","url":null,"abstract":"<div><div>Serum testosterone (T) in males has been declining during the past decades. The previous reports found that 1-nitropyrene (1-NP) exposure suppressed testicular T synthesis. The purpose of the current study was to further explore whether premature senescence participates in 1-NP-triggered reduction of testicular T synthesis. Adult male mice were orally exposed to 1-NP (0, 100, and 500 μg/kg) daily for 14 days. Serum and testicular T contents were diminished in 1-NP-administered mice. Mitochondria-located steroidogenic synthases, including StAR, CYP11A1, and 3βHSD1, were downregulated in 1-NP-administered mouse testes and MLTC-1 cells. Mechanistically, 1-NP exposure increased acetylation modification of mitochondrial steroidogenic synthases by inhibiting the enzymatic activity of SIRT3, an NAD<sup>+</sup>-dependent deacetylase. Supplementing NAD <sup>+</sup> precursor and <em>Sirt3</em> overexpression relieved 1-NP-triggered reduction of steroidogenic synthase levels in mouse testes and MLTC-1 cells. By contrast, <em>Sirt3</em> silencing aggravated 1-NP-evoked acetylation and reduction of steroidogenic synthase levels in MLTC-1 cells. Further experiments demonstrated that 1-NP exposure caused mitochondrial malfunction and premature senescence in mouse testes and MLTC-1 cells. Supplementation with mitochondria-directed antioxidant mitoquinone (MitoQ) prevented 1-NP-evoked Leydig cell premature senescence and downregulation of testicular steroidogenic synthases. These results suggest that mitochondrial malfunction-initiated Leydig cell premature senescence may partially participate in 1-NP-evoked reduction of steroidogenic synthase levels in testes.</div></div>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":null,"pages":null},"PeriodicalIF":7.1,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142461844","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Effect of peroxiredoxin 1 or peroxiredoxin 2 knockout on the thiol proteome of Jurkat cells 过氧化物酶 1 或过氧化物酶 2 基因敲除对 Jurkat 细胞硫醇蛋白质组的影响

IF 7.1 2区生物学

Free Radical Biology and Medicine Pub Date : 2024-10-18 DOI: 10.1016/j.freeradbiomed.2024.10.293

{"title":"Effect of peroxiredoxin 1 or peroxiredoxin 2 knockout on the thiol proteome of Jurkat cells","authors":"","doi":"10.1016/j.freeradbiomed.2024.10.293","DOIUrl":"10.1016/j.freeradbiomed.2024.10.293","url":null,"abstract":"<div><div>Peroxiredoxins are important regulators of cellular peroxide metabolism. As antioxidants, they restrict oxidation of other cell proteins, but as signaling molecules they can act as sensors and promote thiol protein oxidation via a redox relay mechanism. The presence of peroxiredoxins could therefore influence other thiol proteins, even in cells experiencing endogenous redox activity. To investigate this for the two cytoplasmic peroxiredoxins, Prdx1 and Prdx2, we have compared the thiol proteome of wildtype Jurkat cells with cells in which either one was knocked out. Using mass spectrometry and isotope tagging, approximately 10,000 common CysSH-containing peptides were detected for each WT/KO comparison. Knockout of Prdx1 or Prdx2 resulted in a change in redox state of a small selection of Cys residues, with less than 100 giving more than a 2-fold difference. Strikingly, a large proportion of these, including those that showed the greatest change, were common to both KOs. Some Cys residues showed more oxidation in the knockouts, whereas others showed less. The candidate proteins have diverse functions and have not been known to be oxidant sensitive. No differences were seen in redox state of Cys residues of other Prdxs and oxidant sensitive proteins. A change in expression in Prdx2 knockout cells was indicated for seven cytoskeletal or regulatory thiol proteins, three of which were tested and validated by western blotting. Little firm evidence was found for thiol redox changes dependent on either Prdx that could be attributed to oxidation via a relay mechanism.</div></div>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":null,"pages":null},"PeriodicalIF":7.1,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142461733","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Therapeutic potential of plasma-treated solutions in atopic dermatitis 等离子处理液对特应性皮炎的治疗潜力

IF 7.1 2区生物学

Free Radical Biology and Medicine Pub Date : 2024-10-18 DOI: 10.1016/j.freeradbiomed.2024.10.290

{"title":"Therapeutic potential of plasma-treated solutions in atopic dermatitis","authors":"","doi":"10.1016/j.freeradbiomed.2024.10.290","DOIUrl":"10.1016/j.freeradbiomed.2024.10.290","url":null,"abstract":"<div><div>Atopic Dermatitis (AD) is a prevalent inflammatory skin disease that is currently incurable. Plasma-treated solutions (PTS) (e.g., culture media, water, or normal saline, previously exposed to plasma) are being studied as novel therapy. Recently, PTS is gaining attention due to its advantages over non-thermal plasma (also known as cold atmospheric plasma). Thus, we explore the application of PTS in treating AD. In vivo experiments demonstrated that PTS significantly alleviated AD-like symptoms. It reduced mast cell and macrophage infiltration, decreased scratching times and serum IgE levels. These therapeutic effects of PTS on AD mice were associated with the activation of the antioxidant molecule Nrf2. In vitro experiments revealed that PTS could decrease ROS level and regulate cytokine expression (such as IL-6, IL-10, IL-13 and CCL17) in TNF-α/IFN-γ-stimulated keratinocytes and LPS-stimulated M1 macrophages. Additionally, PTS could upregulate the expression of antioxidant stress molecules such as Nrf2, HO-1, NQO1 and PPAR-γ in both cell types. Overall, PTS demonstrated potent therapeutic potential for AD without notable side effects. Our research provided a promising approach to AD treatment and may serve as a potential therapeutic strategy in other inflammatory skin diseases.</div></div>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":null,"pages":null},"PeriodicalIF":7.1,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142461756","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Exercise-induced adaptations to homeostasis of reactive oxygen species in skeletal muscle 运动引起的骨骼肌活性氧平衡适应。

IF 7.1 2区生物学

Free Radical Biology and Medicine Pub Date : 2024-10-18 DOI: 10.1016/j.freeradbiomed.2024.10.270

引用次数: 0

Insufficient S-sulfhydration of serum and glucocorticoid-regulated kinase 1 participates in hyperhomocysteinemia-induced liver injury 血清和糖皮质激素调控激酶 1 的 S-脱水不足参与高同型半胱氨酸血症诱发的肝损伤

IF 7.1 2区生物学

Free Radical Biology and Medicine Pub Date : 2024-10-18 DOI: 10.1016/j.freeradbiomed.2024.10.294

{"title":"Insufficient S-sulfhydration of serum and glucocorticoid-regulated kinase 1 participates in hyperhomocysteinemia-induced liver injury","authors":"","doi":"10.1016/j.freeradbiomed.2024.10.294","DOIUrl":"10.1016/j.freeradbiomed.2024.10.294","url":null,"abstract":"<div><h3>Background & aims</h3><div>Previous studies have established that hyperhomocysteinemia (HHcy) significantly contributes to the development of non-alcoholic steatohepatitis (NASH). Conversely, hydrogen sulfide (H<sub>2</sub>S) has shown potential in mitigating NASH. Despite these findings, it remains uncertain whether H<sub>2</sub>S can serve as a therapeutic agent against HHcy-induced liver damage.</div></div><div><h3>Methods</h3><div>Mice were fed a high-methionine diet to induce HHcy and HepG2 cells were exposed to homocysteine (Hcy). In both models, we assessed liver injury, H<sub>2</sub>S concentration, and autophagy levels. For rescue, sodium hydrosulfide (NaHS), an H<sub>2</sub>S donor, was used to test its potential in reversing hepatic pathological features induced by HHcy.</div></div><div><h3>Results</h3><div>1) Hcy accumulation led to liver damage and increased autophagy. This was linked to insufficient S-sulfhydration of serum and glucocorticoid-regulated kinase 1 (SGK1) at Cys244 and Cys282, a crucial autophagy regulator. The deficiency in S-sulfhydration was resulted from downregulation of cystathionine-γ-lyase (CSE) and subsequent H<sub>2</sub>S decrease, leading to SGK1 inactivation. 2) Administration of NaHS reduced the liver damage caused by high Hcy levels and restored H<sub>2</sub>S levels, promoting the S-sulfhydration and activation of SGK1. 3) Pharmacological inhibition of SGK1 induced autosis, a specific type of cell death caused by overactivation of autophagy. Conversely, a constitutively active mutant of SGK1 (SGK1<sup>S422D</sup>) significantly decreased autophagy and improved cell viability.</div></div><div><h3>Conclusions</h3><div>NaHS supplementation mitigates HHcy-induced liver injury by downregulating hepatic autophagy through the S-sulfhydration and activation of SGK1. This post-translational modification by H<sub>2</sub>S holds promise as a therapeutic approach for HHcy-induced liver injury.</div></div>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":null,"pages":null},"PeriodicalIF":7.1,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142461736","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Mesenchymal stromal cells deliver H2S-enhanced Nrf2 via extracellular vesicles to mediate mitochondrial homeostasis for repairing hypoxia-ischemia brain damage 间充质基质细胞通过细胞外囊泡输送H2S增强的Nrf2，以介导线粒体平衡，从而修复缺氧缺血性脑损伤。

IF 7.1 2区生物学

Free Radical Biology and Medicine Pub Date : 2024-10-18 DOI: 10.1016/j.freeradbiomed.2024.10.292

{"title":"Mesenchymal stromal cells deliver H2S-enhanced Nrf2 via extracellular vesicles to mediate mitochondrial homeostasis for repairing hypoxia-ischemia brain damage","authors":"","doi":"10.1016/j.freeradbiomed.2024.10.292","DOIUrl":"10.1016/j.freeradbiomed.2024.10.292","url":null,"abstract":"<div><div>Mesenchymal stromal cells (MSCs) are considered a therapeutic approach for neurological diseases via extracellular vesicles (EVs). Modified EVs contain active components with enhanced therapeutic potential. In this study, we aimed to explore the role and underlying mechanism of EVs from MSCs preconditioned by NaHS (an Hydrogen sulfide donor) (H<sub>2</sub>S-EVs) in hypoxia-ischemia (HI) brain damage. Our results showed that H<sub>2</sub>S-EVs treatment via the non-invasive intranasal route in HI mice was able to reduce oxidative stress and mitochondrial dysfunction compared to EVs treatment. Mechanistic studies demonstrated that NaHS promoted nuclear factor erythroid-2 related factor 2 (Nrf2) expression in the cytoplasm by inducing Parkinson disease protein 7 (PARK7)‐dependent disintegration of Nrf2/Keap-1 complex in MSCs. In particular, the free Nrf2 was loaded into the EVs as a result of its KFERQ motif being recognized by 70-kDa heat shock proteins and lysosomal-associated membrane protein 2A. Subsequently, H<sub>2</sub>S-EVs were internalized into neurons in the ipsilateral hemisphere, thus delivering abundant Nrf2 to accumulate in the mitochondria and remodeling mitochondrial function following H<sub>2</sub>S-EVs treatment in HI mice. Moreover, Nrf2 knockdown in MSCs remarkably impaired H<sub>2</sub>S-EVs-mediated therapeutic effects on HI mice. In brief, the present study for the first time demonstrated that H<sub>2</sub>S-modified MSCs significantly accumulated higher Nrf2 in EVs via upregulating PARK7 expression, revealing the mechanism through which antioxidant protein Nrf2 delivered by H<sub>2</sub>S-EVs protect against mitochondrial dysfunction in HI brain damage.</div></div>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":null,"pages":null},"PeriodicalIF":7.1,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142461737","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Renal microRNA-144-3p is associated with transforming growth factor-β1-induced oxidative stress and fibrosis by suppressing the NRF2 pathway in hypertensive diabetic kidney disease 肾脏 microRNA-144-3p 通过抑制高血压糖尿病肾病患者的 NRF2 通路，与转化生长因子-β1 诱导的氧化应激和纤维化有关。

IF 7.1 2区生物学

Free Radical Biology and Medicine Pub Date : 2024-10-17 DOI: 10.1016/j.freeradbiomed.2024.10.286

{"title":"Renal microRNA-144-3p is associated with transforming growth factor-β1-induced oxidative stress and fibrosis by suppressing the NRF2 pathway in hypertensive diabetic kidney disease","authors":"","doi":"10.1016/j.freeradbiomed.2024.10.286","DOIUrl":"10.1016/j.freeradbiomed.2024.10.286","url":null,"abstract":"<div><div>Chronic kidney disease (CKD) is a global health problem characterized by progressive renal fibrosis and excessive extracellular matrix deposition. Oxidative stress and epigenetic regulation, particularly through microRNAs (miRNAs), play crucial roles in the pathogenesis of CKD. In this study, we investigated the role of urinary miR-144-3p, which is upregulated in rats with CKD induced by diabetes and hypertension, in renal fibrosis progression, particularly its regulation of the nuclear factor erythroid-2-related factor 2 (NRF2) pathway. Our findings revealed elevated miR-144-3p levels and reduced NRF2 and target gene levels in kidney tissues of streptozotocin-treated spontaneously hypertensive rats. <em>In vitro</em> experiments demonstrated that miR-144-3p directly binds to the 3′-untranslated region of <em>nrf2</em>, suppressing the NRF2 pathway in renal tubular epithelial cells. Additionally, the profibrogenic factor transforming growth factor (TGF)-β1 increased miR-144-3p expression. TGF-β1-induced NRF2 suppression and reactive oxygen species elevation were found to be mediated through miR-144-3p upregulation. <em>In vivo</em>, cilostazol, an antiplatelet drug with an NRF2-activating effect, ameliorated renal injury in diabetic hypertensive rats by decreasing TGF-β1 and miR-144-3p levels while increasing NRF2 and its target gene levels in the kidneys. These findings highlight the potential therapeutic value of targeting the miR-144-3p/NRF2 pathway to attenuate CKD progression in hypertensive diabetic conditions.</div></div>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":null,"pages":null},"PeriodicalIF":7.1,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142461740","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Mouse models used to test the role of reactive oxygen species in aging and age-related chronic diseases 用于测试活性氧在衰老和与年龄相关的慢性疾病中的作用的小鼠模型。

IF 7.1 2区生物学

Free Radical Biology and Medicine Pub Date : 2024-10-16 DOI: 10.1016/j.freeradbiomed.2024.10.269

引用次数: 0