Redox Biology最新文献

{"title":"PDE4D inhibition ameliorates cardiac hypertrophy and heart failure by activating mitophagy","authors":"Jing Fu ,&nbsp;Congping Su ,&nbsp;Yin Ge ,&nbsp;Zhou Ao ,&nbsp;Li Xia ,&nbsp;Yingxiang Chen ,&nbsp;Yizheng Yang ,&nbsp;Shiwei Chen ,&nbsp;Rui Xu ,&nbsp;Xiaoyan Yang ,&nbsp;Kai Huang ,&nbsp;Qin Fu","doi":"10.1016/j.redox.2025.103563","DOIUrl":"10.1016/j.redox.2025.103563","url":null,"abstract":"<div><div>Cyclic adenosine monophosphate (cAMP) plays a major role in normal and pathologic signaling in the heart. Phosphodiesterase 4 (PDE4) is a major PDE degrading cAMP in the heart. There are inconsistencies concerning the roles of the PDE4 isoforms 4B and 4D in regulation of cardiac function. Cardiac PDE4B overexpression is beneficial in remodeling and heart failure (HF), however, the effect of PDE4D and PDE4 inhibitor in HF remains unclear. We generated global and conditional cardiac-specific heterozygous PDE4D knockout mice and adeno-associated virus serotype 9-PDE4D overexpression to determine the role of PDE4D in cardiac hypertrophy and HF. PDE4D upregulation was observed in failing hearts from human and isoproterenol injection and TAC mice. <em>In vitro</em>, isoproterenol stimulation increased PDE4D expression via PKA but had no effect on PDE4B expression in cardiomyocytes. PDE4D overexpression per se induced oxidative stress, mitochondrial damage and cardiomyocyte hypertrophy by decreasing PINK1/Parkin-mediated mitophagy through inhibiting cAMP-PKA-CREB-Sirtuin1 (SIRT1) signaling pathway, while PDE4B overexpression did not affect CREB-SIRT1 pathway and mitophagy but exhibited a protective effect on isoproterenol-induced oxidative stress and hypertrophy in cardiomyocytes. PDE4D silencing or inhibition with PDE4 inhibitor roflumilast ameliorated isoproterenol-induced mitochondrial injury and cardiomyocyte hypertrophy. <em>In vivo</em>, ISO injection or TAC inhibited cardiac mitophagy and caused cardiac hypertrophy and HF, which were ameliorated by roflumilast or cardiac-specific PDE4D haploinsufficiency. Conversely, cardiac PDE4D overexpression suppressed cardiac mitophagy and abolished the protective effects of global PDE4D haploinsufficiency on TAC-induced cardiac hypertrophy and HF. In conclusion, these studies elucidate a novel mechanism by which sustained adrenergic stimulation contributes to cardiac hypertrophy and HF by increasing PDE4D via cAMP-PKA signaling, which in turn reduces cAMP-PKA activity, resulting in cardiomyocyte hypertrophy and mitochondrial injury via inhibition of CREB-SIRT1 signaling-mediated mitophagy. PDE4D inhibition may represent a novel therapeutic strategy for HF.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"81 ","pages":"Article 103563"},"PeriodicalIF":10.7,"publicationDate":"2025-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143487352","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Redox imbalance drives magnetic property and function changes in mice","authors":"Chuanlin Feng ,&nbsp;Lei Zhang ,&nbsp;Xiaoyuan Zhou ,&nbsp;Shiyu Lu ,&nbsp;Ruowen Guo ,&nbsp;Chao Song ,&nbsp;Xin Zhang","doi":"10.1016/j.redox.2025.103561","DOIUrl":"10.1016/j.redox.2025.103561","url":null,"abstract":"<div><div>The magnetic properties of substances directly determine their response to an externally applied magnetic field, which are closely associated with magnetoreception, magnetic resonance imaging (MRI), and magnetic bioeffects. However, people's understanding of the magnetic properties of living organisms remains limited. In this study, we utilized <em>NRF2</em> (nuclear factor erythroid 2-related factor 2) deficient mice to investigate the contribution of redox (oxidation–reduction) homeostasis, in which the key process is the transfer of electron, a direct target of magnetic field and origin of paramagnetism. Our results show that the <em>NRF2</em>^{<em>−/−</em>} mice exhibit significantly altered systemic redox state, accompanied by increased magnetic susceptibility, particularly in the liver and spleen. Further analyses reveal that the levels of paramagnetic reactive oxygen species (ROS) in these tissues are markedly elevated compared to wild-type mice. Moreover, the concentrations of Fe²⁺ and Fe³⁺ are significantly elevated in <em>NRF2</em>^{<em>−/−</em>} mice, which are directly correlated with the increased magnetic susceptibility. The disrupted redox balance in <em>NRF2</em>^{<em>−/−</em>} mice not only exacerbates oxidative stress and iron deposition, but also induces impairment to the liver and spleen. The findings highlight the combined effects of ROS and iron metabolism in driving magnetic susceptibility changes, providing valuable theoretical insights for further research into magnetic bioeffects and organ-specific sensitivity to magnetic fields.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"81 ","pages":"Article 103561"},"PeriodicalIF":10.7,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143508697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of Tie2 as a sensor for reactive oxygen species and its therapeutic implication","authors":"An Vuong Quynh Pham ,&nbsp;Yongwoo Na ,&nbsp;Gyeongseo Suk ,&nbsp;Chansik Yang ,&nbsp;So Min Kang ,&nbsp;Joonha Lee ,&nbsp;Hongseo Choi ,&nbsp;Wook Kim ,&nbsp;Sung Wook Chi ,&nbsp;Sangyeul Han ,&nbsp;Hae Woong Choi ,&nbsp;Hyeonwoo Kim ,&nbsp;Chungho Kim","doi":"10.1016/j.redox.2025.103555","DOIUrl":"10.1016/j.redox.2025.103555","url":null,"abstract":"<div><div>Psoriasis is a chronic inflammatory disease characterized by hyperproliferation of keratinocytes and abnormal blood vessels. As hyperproliferation is driven by pro-inflammatory cytokines produced by activated immune cells, therapeutic strategies often target these cytokines to manage the disease. However, the role of abnormally developed blood vessels has often been overlooked in treatment approaches. In this study, we focused on blood vessels in psoriatic lesions and investigated the potential interplay between immune and endothelial cells by adopting imiquimod treated mice as <em>in vivo</em> model, together with various cell biological, biochemical, and structural analyses. We found that activated immune cells can generate reactive oxygen species, subsequently inducing oxidative stress in endothelial cells. Oxidative stress impairs endothelial cell layer integrity, thereby facilitating transendothelial migration of immune cells. Mechanistically, oxidative conditions inhibit Tie2 activation, potentially by modifying its cysteine residues, leading to deactivation of its vessel-stabilizing functions. Additionally, we demonstrated that reactivating Tie2 under such conditions could restore endothelial barrier function and alleviate the disease. These results suggest that Tie2 serves as a receptor that is directly responsive to oxidative environments, thereby modulating its kinase activity. Furthermore, we suggest that Tie2 reactivation is a promising alternative therapeutic approach for psoriasis.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"81 ","pages":"Article 103555"},"PeriodicalIF":10.7,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143474681","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Estrogen metabolites and hydrogen peroxide - Missing elements in the pathophysiology and possible treatment of treatment-resistant depression?","authors":"Zofia Winczewska ,&nbsp;Agnieszka Mechlińska ,&nbsp;Piotr Radziwiłłowicz ,&nbsp;Lucyna Konieczna ,&nbsp;Joanna Drzeżdżon ,&nbsp;Dagmara Jacewicz ,&nbsp;Mariusz Wiglusz ,&nbsp;Tomasz Bączek ,&nbsp;Wiesław Jerzy Cubała ,&nbsp;Magdalena Górska-Ponikowska","doi":"10.1016/j.redox.2025.103547","DOIUrl":"10.1016/j.redox.2025.103547","url":null,"abstract":"<div><div>The pathogenesis of depression is complex and heterogeneous, and the management of this disease remains unsatisfactory, so mechanisms and therapeutic strategies are constantly being sought. This study aimed to determine the potential role of estrogen metabolites in the pathogenesis of treatment-resistant depression (TRD) based on the determination of concentrations of estrogens and their metabolites and hydrogen peroxide (H₂0₂) in the biological material of patients with TRD.</div><div>In this study, we observed for the first time an association between unbalanced estrogen metabolism and elevated H₂0₂ levels in TRD patients. Reduced concentrations of 2-methoxyestradiol (2-ME2), 17α-estradiol (α-E2) and 17β-estradiol (β-E2) may be due to abnormal estrogen metabolism toward neurotoxic semiquinones and quinones which are a potential as yet undescribed mechanism responsible for generating oxidative stress (OS) in TRD.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"81 ","pages":"Article 103547"},"PeriodicalIF":10.7,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143580327","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Characterization of the glutathione redox state in the Golgi apparatus","authors":"Carla Miró-Vinyals ,&nbsp;Sarah Emmert ,&nbsp;Gina Grammbitter ,&nbsp;Alex Jud ,&nbsp;Tobias Kockmann ,&nbsp;Pablo Rivera-Fuentes","doi":"10.1016/j.redox.2025.103560","DOIUrl":"10.1016/j.redox.2025.103560","url":null,"abstract":"<div><div>Redox homeostasis is crucial for cell function, and, in eukaryotic cells, studying it in a compartmentalized way is essential due to the redox variations between different organelles. The redox state of organelles is largely determined by the redox potential of glutathione, <em>E</em>_GSH, and the concentration of its reduced and oxidized species, <em>[GS]</em>. The Golgi apparatus is an essential component of the secretory pathway, yet little is known about the concentration or redox state of GSH in this organelle. Here, we characterized the redox state of GSH in the Golgi apparatus using a combination of microscopy and proteomics methods. Our results prove that the Golgi apparatus is a highly oxidizing organelle with a strikingly low GSH concentration (<em>E</em>_GSH = – 157 mV, 1–5 mM). These results fill an important gap in our knowledge of redox homeostasis in subcellular organelles. Moreover, the new Golgi-targeted GSH sensors allow us to observe dynamic changes in the GSH redox state in the organelle and pave the way for further characterization of the Golgi redox state under various physiological and pathological conditions.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"81 ","pages":"Article 103560"},"PeriodicalIF":10.7,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143465416","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Redox regulation of lung endothelial PERK, unfolded protein response (UPR) and proliferation via NOX1: Targeted inhibition as a potential therapy for PAH","authors":"Christian J. Goossen ,&nbsp;Alex Kufner ,&nbsp;Christopher M. Dustin ,&nbsp;Imad Al Ghouleh ,&nbsp;Shuai Yuan ,&nbsp;Adam C. Straub ,&nbsp;John Sembrat ,&nbsp;Jeffrey J. Baust ,&nbsp;Delphine Gomez ,&nbsp;Damir Kračun ,&nbsp;Patrick J. Pagano","doi":"10.1016/j.redox.2025.103554","DOIUrl":"10.1016/j.redox.2025.103554","url":null,"abstract":"<div><h3>Aims</h3><div>Reactive oxygen species (ROS) play an important role in the pathogenesis of pulmonary arterial hypertension (PAH) and NADPH oxidases (NOXs) as sources of ROS are implicated in the development of the disease. We previously showed that NOX isozyme 1 (NOX1)-derived ROS contributes to pulmonary vascular endothelial cell (EC) proliferation in response to PAH triggers <em>in vitro</em>. However, whether and how NOX1 is involved in PAH <em>in vivo</em> have not been explored nor has NOX1 been examined as a viable and effective therapeutic disease target.</div></div><div><h3>Methods and results</h3><div>Herein, infusion of mice exposed to Sugen/hypoxia (10 % O₂) with a specific NOX1 inhibitor, NOXA1ds, delivered via osmotic minipumps (i.p.), significantly suppressed pathological changes in hemodynamic parameters characteristic of PAH. Furthermore, lungs of human patients with idiopathic PAH (iPAH) and exploratory RNA-seq analysis of hypoxic human pulmonary ECs, in which NOX1 was suppressed, were probed. The findings showed a clear indication of NOX1 in the promotion of both protein disulfide isomerase (PDI) and the unfolded protein response (UPR; in particular, the PERK arm of the pathway including eIF2α and ATF4) leading to proliferation. In aggregate, these results are consistent with a causal role for NOX1 in the development of mouse and human PAH and reveal a novel and mechanistic pathway by which NOX1 activates the UPR response during EC proliferation.</div></div><div><h3>Conclusion</h3><div>NOX1 promotes phenotypic changes in ECs that are pivotal to proliferation and PAH through activation of the UPR. Taken together, our results are consistent with selective inhibition of NOX1 as a novel modality for attenuating PAH.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"82 ","pages":"Article 103554"},"PeriodicalIF":10.7,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143705965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oxidized protein aggregate lipofuscin impairs cardiomyocyte contractility via late-stage autophagy inhibition","authors":"Sophia Walter ,&nbsp;Steffen P. Häseli ,&nbsp;Patricia Baumgarten ,&nbsp;Stefanie Deubel ,&nbsp;Tobias Jung ,&nbsp;Annika Höhn ,&nbsp;Christiane Ott ,&nbsp;Tilman Grune","doi":"10.1016/j.redox.2025.103559","DOIUrl":"10.1016/j.redox.2025.103559","url":null,"abstract":"<div><div>Aging of the heart is accompanied by impairment of cardiac structure and function. At molecular level, autophagy plays a crucial role in preserving cardiac health. Autophagy maintains cellular homeostasis by facilitating balanced degradation of cytoplasmic components including organelles and misfolded or aggregated proteins. The age-related decline in autophagy favors an accumulation of protein aggregates such as lipofuscin particularly in the heart, which is composed primarily of non-proliferating cells. Therefore, this study investigates whether lipofuscin accumulation contributes to age-related functional decline of primary adult cardiomyocytes isolated from C57BL/6J mice and examines the role of autophagic flux in mediating these effects.</div><div>Results showed an age-associated reduction in cardiomyocyte contraction amplitude and an increase in autofluorescence, indicating the accumulation of lipofuscin with age. <em>In vitro</em> treatment of adult primary cardiomyocytes with artificial lipofuscin increased autofluorescence and decreased both contraction amplitude and cellular autophagic flux. Induction of autophagy with rapamycin mitigated contractile dysfunction in lipofuscin-treated cardiomyocytes, whereas inhibition of autophagic flux revealed stage-dependent effects. Late-stage autophagy inhibition using chloroquine or concanamycin A reduced cardiomyocyte contraction amplitude, whereas early-stage autophagy inhibition via 3-methyladenine did not affect contraction within 24 h.</div><div>In conclusion, our results indicate that lipofuscin directly impairs cardiomyocyte function by diminishing late-stage autophagic flux. These findings highlight the essential role of the autophagy-lysosomal system in preserving age-related loss of cardiomyocyte function caused by accumulating protein aggregates.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"81 ","pages":"Article 103559"},"PeriodicalIF":10.7,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143594087","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Quercetin alleviates LPS/iE-DAP-induced liver injury by suppressing ferroptosis via regulating ferritinophagy and intracellular iron efflux","authors":"Hongzhu Zhang,&nbsp;Huimin Shi,&nbsp;Xuerui Li,&nbsp;Shendong Zhou,&nbsp;Xiaokun Song,&nbsp;Nana Ma,&nbsp;Meijuan Meng,&nbsp;Guangjun Chang,&nbsp;Xiangzhen Shen","doi":"10.1016/j.redox.2025.103557","DOIUrl":"10.1016/j.redox.2025.103557","url":null,"abstract":"<div><div>Ruminal dysbiosis-induced liver injury is prevalent in dairy cows, yet its underlying mechanisms remain incompletely understood. Ferroptosis, a newly identified form of programmed cell death distinct from apoptosis and necrosis, has been implicated in various liver diseases by emerging studies. In the present study, lipopolysaccharide (LPS) and γ-D-glutamyl‐meso‐diaminopimelic acid (iE-DAP) were employed to establish <em>in vitro</em> and <em>in vivo</em> models of liver injury using bovine hepatocytes and mice, respectively. It was observed that noncytotoxic iE-DAP alone did not influence lipid peroxidation or GPX4, but exacerbated LPS-induced ferroptosis and hepatocyte injury. Notably, co-treatment with LPS and iE-DAP (LPS/iE-DAP)-induced hepatocyte injury was mitigated by intervention with the ferroptosis inhibitor ferrostatin-1 (Fer-1). Mechanistically, the activated IL-6/STAT3 signaling pathway was found to mediate LPS/iE-DAP-induced ferroptosis. Suppression of IL-6/STAT3, either through <em>IL6</em> and <em>STAT3</em> knockdown or pharmacological intervention, reduced Fe²⁺ accumulation and alleviated ferroptotic cell death. Further investigations identified that IL-6/STAT3 signaling enhanced ferritinophagy and impaired iron export. Either disrupting ferritinophagy by knocking down <em>NCOA4</em> or restoring iron export via <em>HAMP</em> knockdown relieved intracellular iron overload and inhibited ferroptosis. Specifically, LPS/iE-DAP treatment increased the interaction between hepcidin and ferroportin, promoting ferroportin ubiquitination and degradation, thereby blocking iron efflux. Furthermore, we provided several evidence to prove that quercetin pretreatment alleviated LPS/iE-DAP-induced ferroptosis and liver injury by decreasing hepatic iron accumulation via targeting the IL-6/STAT3 signaling <em>in vitro</em> and <em>in vivo</em>, effects reversed by the addition of recombinant bovine IL-6. Based on these findings, we concluded that LPS/iE-DAP-induced liver injury by triggering ferroptosis through regulating IL-6/STAT3/ferritinophagy-dependent iron release and IL-6/STAT3/hepcidin/ferroportin-dependent iron export, while quercetin could alleviate this liver injury by inhibiting ferroptosis via IL-6/STAT3 signaling pathway. This study provides novel insights into the mechanisms whereby ruminal dysbiosis induces liver injury and presents a prospective solution for ruminal dysbiosis-induced liver injury.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"81 ","pages":"Article 103557"},"PeriodicalIF":10.7,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143452962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mesenchymal stem cell-derived extracellular vesicles attenuate ferroptosis in aged hepatic ischemia/reperfusion injury by transferring miR-1275","authors":"Yihang Gong ,&nbsp;Qiang You ,&nbsp;Xiaofeng Yuan ,&nbsp;Fanxin Zeng ,&nbsp;Feng Zhang ,&nbsp;Jiaqi Xiao ,&nbsp;Haitian Chen ,&nbsp;Yasong Liu ,&nbsp;Tingting Wang ,&nbsp;Xijing Yan ,&nbsp;Wenjie Chen ,&nbsp;Yingcai Zhang ,&nbsp;Qi Zhang ,&nbsp;Jia Yao ,&nbsp;Jiebin Zhang ,&nbsp;Rong Li ,&nbsp;Jun Zheng","doi":"10.1016/j.redox.2025.103556","DOIUrl":"10.1016/j.redox.2025.103556","url":null,"abstract":"<div><div>With an aging global population, the proportion of aged donor livers in graft pools is steadily increasing. Compared to young livers, aged livers exhibit heightened susceptibility to hepatic ischemia/reperfusion injury (HIRI), which significantly limits their utilisation in liver transplantation (LT) and exacerbates organ shortages. Our previous study demonstrated that ferroptosis is a pivotal trigger for HIRI vulnerability in aged livers. However, effective clinical strategies for the inhibition of ferroptosis remain elusive. Utilizing an aged mouse HIRI model, primary hepatocytes, and human liver organoids, this study provides hitherto undocumented evidence that mesenchymal stem cell-derived extracellular vesicles (MSC-EVs) effectively alleviate HIRI in aged livers by inhibiting ferroptosis. Mechanistically, miR-1275, which was significantly enriched within MSC-EVs, was transferred to hepatocytes. Subsequently, miR-1275 downregulated the expression of SLC39A14, a crucial iron transporter that is upregulated in aged livers and plays a pivotal role in promoting ferroptosis. Furthermore, we found a negative correlation between SLC39A14 levels and prognosis of aged donor liver recipients using clinical LT samples. Silencing miR-1275 in MSC-EVs or modulating SLC39A14 levels in aged livers reversed MSC-EV-mediated mitigation of ferroptosis. Collectively, these findings revealed the novel therapeutic potential of MSC-EVs in attenuating aged HIRI, suggesting a promising treatment for improving prognosis and preventing serious complications in recipients of aged liver grafts during LT.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"81 ","pages":"Article 103556"},"PeriodicalIF":10.7,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143452961","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “Aspirin promotes RSL3-induced ferroptosis by suppressing mTOR/SREBP-1/SCD1-mediated lipogenesis in PIK3CA-mutatnt colorectal cancer” [Redox Biol. 55 (2022) 102426]","authors":"Hao Chen ,&nbsp;Qinqin Qi ,&nbsp;Nan Wu ,&nbsp;Ying Wang ,&nbsp;Qian Feng ,&nbsp;Rong Jin ,&nbsp;Lei Jiang","doi":"10.1016/j.redox.2025.103533","DOIUrl":"10.1016/j.redox.2025.103533","url":null,"abstract":"","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"80 ","pages":"Article 103533"},"PeriodicalIF":10.7,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143426064","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}