抗氧化剂和氧化还原信号 (ARS) 是领先的同行评审期刊，致力于了解氧气和氧化还原 (氧化还原) 过程对人类健康和疾病的重要影响。该杂志探讨了基于遗传、药物和营养氧化还原疗法的关键问题。前沿研究侧重于结构生物学、干细胞、再生医学、表观遗传学、影像学、临床结果以及预防和治疗营养学等领域。ARS 已扩展到在一本期刊中创建两个独特的焦点：ARS DISCOVERIES 和 ARS THERAPEUTICS。 ARS DISCOVERIES（24 期）发表基础和应用研究领域的最高水平突破。 ARS THERAPEUTICS（12 期）是同类出版物中的第一本，它将通过展示氧化还原科学改变健康结果的潜力来帮助增强整个氧化还原生物学领域。ARS 覆盖范围包括：-ROS/RNS 作为信使-气体信号传感器-缺氧和组织氧合-MICRORNA-原核系统-植物生物学的教训

Antioxidants and Redox Signaling is a leading peer-reviewed journal dedicated to understanding the significant impact of oxygen and redox processes on human health and disease. The journal explores key issues related to genetic, pharmacological, and nutritional redox therapies. Cutting-edge research focuses on areas such as structural biology, stem cells, regenerative medicine, epigenetics, imaging, clinical outcomes, and preventive and therapeutic nutrition. The journal has expanded to create two unique focuses: ARS DISCOVERIES and ARS THERAPEUTICS. ARS DISCOVERIES (24 issues) publishes high-level breakthroughs in basic and applied research, while ARS THERAPEUTICS (12 issues) is the first of its kind, aimed at enhancing the entire field of redox biology by showcasing the potential of redox science to improve health outcomes. The scope of ARS includes: - ROS/RNS as messengers - Gas signaling sensors - Hypoxia and tissue oxygenation - MicroRNA - Prokaryotic systems - Lessons from plant biology.

《Antioxidants and Redox Signaling》是一本领先的同行评审期刊，专注于氧气及氧化还原过程对人类健康和疾病的重要影响。该期刊探讨了与遗传、药物和营养相关的氧化还原疗法的关键问题。前沿研究涵盖结构生物学、干细胞、再生医学、表观遗传学、影像学、临床结果以及预防和治疗营养学等领域。期刊分为两个独特的焦点：ARS DISCOVERIES 和 ARS THERAPEUTICS。ARS DISCOVERIES（24期）发表基础和应用研究领域的重大突破，而ARS THERAPEUTICS（12期）是同类出版物中的首个，通过展示氧化还原科学在改善健康结果方面的潜力，推动整个氧化还原生物学领域的发展。ARS的研究范围包括：- ROS/RNS作为信使 - 气体信号传感器 - 缺氧与组织氧合 - 微小RNA - 原核系统 - 植物生物学的启示

Antioxidants and Redox Signaling

Reactive oxygen species (ROS) and cellular oxidative stress are involved in many physiological and pathophysiological processes, including cellular and organismal aging, migration, proliferation, senescence or death of normal and cancer cells, and stress resistance of stem cells. The forkhead homeobox type O (FOXO) transcription factors FOXO1, FOXO3a, and FOXO4 are critical mediators of the cellular responses to oxidative stress and have been implicated in many of the above ROS-regulated processes. In cancer cells they converge oxidative stress signaling to cell cycle arrest and cell death or promote a motile phenotype. Dependent on their posttranslational modifications FOXOs can also actively regulate the detoxification of cells from ROS and promote stress resistance. Thus, FOXO transcription factors are of vital importance in processes regulating tumor survival or progression, stem cell maintenance, age-related pathological processes, and lifespan extension. Antioxid. Redox Signal. 14, 593–605.

Peter Storz

Forkhead Homeobox Type O Transcription Factors in the Responses to Oxidative Stress

氧化应激反应中的叉头框O型转录因子

Butyrate is a short-chain fatty acid that arrests growth of various types of cells. H2S can be endogenously produced by cystathionine γ-lyase (CSE) or cystathionine β-synthase (CBS) or both in colonic tissues. In this study, we observed endogenous H2S production in a colon cancer cell line (WiDr) and colonic tissues through the activity of both CSE and CBS. After 24 h of incubation of WiDr cells, butyrate increased cell production of H2S and upregulated CBS and CSE expressions. Both butyrate and NaHS (a H2S donor) decreased cell viability in a dose-dependent manner. Blockade of CBS, but not CSE, decreased butyrate-stimulated H2S production and reversed butyrate-inhibited cell viability. In addition, NaHS treatment stimulated the phosphorylation of extracellular signal-regulated kinase (ERK) and p38 mitogen–activated protein kinase (MAPK), but not c-Jun N-terminal kinase (JNK). Inhibition of the phosphorylation of either p38 MAPK or ERK did not abolish NaHS-induced cell death. Butyrate treatment increased the phosphorylation of ERK, not p38 MAPK and JNK, but inhibition of ERK and p38 MAPK phosphorylation did not inhibit butyrate-reduced cell viability. In conclusion, butyrate regulates endogenous H2S production by stimulating CBS expression in colon cancer cells, but butyrate and H2S inhibit cancer cell growth through different mechanisms. Antioxid. Redox Signal. 12, 0000–0000.

Qiuhui Cao

Li Zhang

Guangdong Yang

Changqing Xu

Rui Wang

Antioxidants & Redox Signaling

Butyrate-stimulated H<sub>2</sub>S Production in Colon Cancer Cells

丁酸刺激结肠癌细胞中硫化氢的产生

The development of multidrug resistance to cancer chemotherapy is a major obstacle to the effective treatment of human malignancies. It has been established that membrane proteins, notably multidrug resistance (MDR), multidrug resistance protein (MRP), and breast cancer resistance protein (BCRP) of the ATP binding cassette (ABC) transporter family encoding efflux pumps, play important roles in the development of multidrug resistance. Overexpression of these transporters has been observed frequently in many types of human malignancies and correlated with poor responses to chemotherapeutic agents. Evidence has accumulated showing that redox signals are activated in response to drug treatments that affect the expression and activity of these transporters by multiple mechanisms, including (a) conformational changes in the transporters, (b) regulation of the biosynthesis cofactors required for the transporter's function, (c) regulation of the expression of transporters at transcriptional, posttranscriptional, and epigenetic levels, and (d) amplification of the copy number of genes encoding these transporters. This review describes various specific factors and their relevant signaling pathways that are involved in the regulation. Finally, the roles of redox signaling in the maintenance and evolution of cancer stem cells and their implications in the development of intrinsic and acquired multidrug resistance in cancer chemotherapy are discussed.

Macus Tien Kuo

Redox Regulation of Multidrug Resistance in Cancer Chemotherapy: Molecular Mechanisms and Therapeutic Opportunities

癌症化疗中多药耐药性的氧化还原调控：分子机制与治疗机遇

Significance: Ferroptosis is featured by the accumulation of polyunsaturated-lipid peroxidation on cellular membranes in an iron-dependent manner. Ferroptosis has been implicated in various pathophysiological processes, including cancer, neurodegeneration, and ischemia-reperfusion tissue injury. However, our understanding about the dynamic and context-specific regulation of ferroptosis remains incomplete. Recent Advances: As the major substrate for peroxidation, the cellular lipidome regulates ferroptosis sensitivity and execution by controlling the abundance and availability of polyunsaturated-lipids for peroxidative modifications. In turn, the cellular lipidome is regulated by a complex network of enzymes and transporters, as well as upstream layers of receptors, kinases, and transcription factors. A number of research has shed light on the link between lipid metabolism and ferroptosis. Here, we summarize our current knowledge on the role of the lipidome and associated protein regulators in various stages of ferroptosis, ranging from initiation, execution to cell death evasion by cells experiencing ferroptotic stress. Critical Issues: This review provides an overview of the mechanisms underlying lipid peroxidation and ferroptosis by discussing the lipid species that directly contribute to lipid peroxidation and ferroptosis, how cells regulate the abundances of these pro-ferroptosis lipids, how lipid peroxidation causes cell death, and how cells prevent and repair membrane lipid damage under ferroptotic conditions. Future Directions: Cell fate regulation in vivo could be different from in vitro culture settings. We envision that a comprehensive and detailed understanding about these important questions in the dynamic regulation of ferroptosis in vivo will accelerate our development of ferroptosis-targeted therapies to improve human health.

Nathchar Naowarojna

Tianshu William Wu

Zijian Pan

Mengyu Li

Jingrong Regina Han

Yilong Zou

Antioxidants &amp; Redox Signaling

Dynamic Regulation of Ferroptosis by Lipid Metabolism

脂质代谢对铁死亡的动态调控

SIGNIFICANCE
Ferroptosis, a form of regulated cell death characterized by a large amount of lipid peroxidation-mediated membrane damage, joins the evolution of multisystem diseases. For instance, neurodegenerative diseases, chronic obstructive pulmonary disease and acute respiratory distress syndrome, osteoporosis and osteoarthritis, and so on. Since being identified as the third gasotransmitter in living organisms, the intricate role of hydrogen sulfide (H2S) in ferroptosis has emerged at the forefront of research.


RECENT ADVANCES
The discovery of novel targets in the relevant metabolic pathways, including transferrin receptor 1, cystine/glutamate antiporter, and others, coupled with the exploration of new signaling pathways, particularly the p53 signaling pathway and the nitric oxide / nuclear factor erythroid 2-related factor 2 signaling pathway, and so on. Many diseases such as emphysema and airway inflammation, myocardial diseases, endothelial dysfunction in aging arteries, and traumatic brain injury have recently been found to be alleviated directly by H2S inhibition of ferroptosis. Safe, effective, and tolerable novel H2S donors have been developed and have shown promising results in phase I clinical trials.


CRITICAL ISSUES
Complicated crosstalk between ferroptosis signaling pathway and oncogenic factors results in the risk of cancer when inhibiting ferroptosis. Notably, targeted delivery of H2S is still a challenging task.


FUTURE DIRECTIONS
Discovering more reliable and stable novel H2S donors and achieving their targeted delivery will enable further clinical trials for diseases associated with ferroptosis inhibition by H2S, determining their safety, efficacy, and tolerance.

Yi-Wen Zhu

Zi-Tao Liu

Ao-Qi Tang

Xiao-Yi Liang

Yan Wang

Ya-Fang Liu

Yu-Qing Jin

Wei Gao

Hang Yuan

Da-Yong Wang

Xin-Ying Ji

Dong-Dong Wu

The Emerging Roles of Hydrogen Sulfide in Ferroptosis

氢硫化物在铁死亡中的新兴作用

Alterations of mitochondrial bioenergetics and arginine metabolism are universally present and mechanistically linked to pulmonary arterial hypertension (PAH), but there is little knowledge of arginine metabolism and mitochondrial functions across the different pulmonary hypertension (PH) groups. We hypothesize that abnormalities in mitochondrial functions are present across all PH groups and associated with clinical phenotypes. We test the hypothesis in PH patients and healthy controls from the Pulmonary Vascular Disease Phenomics Program cohort, who had comprehensive clinical phenotyping and follow-up for at least 4 years for death or transplant status. Mitochondrial transmembrane potential, superoxide production, and mass were measured by flow cytometry in fresh platelets. Metabolomics analysis was performed on plasma samples. Global arginine bioavailability was calculated as the ratio of arginine/(ornithine+citrulline).

Samar Farha

Kewal Asosingh

Paul M. Hassoun

John Barnard

Suzy Comhair

Andrew Reichard

Nicholas Wanner

Milena Radeva

Micheala A. Aldred

Gerald J. Beck

Erika Berman-Rosenzweig

Barry A. Borlaug

J. Emanuel Finet

Robert P. Frantz

Gabriele Grunig

Anna R. Hemnes

Nicholas Hill

Evelyn M. Horn

Christine Jellis

Jane A. Leopold

Reena Mehra

Margaret M. Park

Franz P. Rischard

W. H. Wilson Tang

Serpil C. Erzurum

Alterations in Mitochondrial Function in Pulmonary Vascular Diseases

肺血管疾病中线粒体功能的改变

Weizhuo Lu

Jiyue Wen

Anti-Inflammatory Effects of Hydrogen Sulfide in Axes Between Gut and Other Organs

硫化氢在肠道与其他器官轴中的抗炎作用

The role of the canonical transient receptor potential 6 (TRPC6) channel in chronic obstructive pulmonary disease (COPD) remains poorly understood at the mechanistic level.

Kun Liu

Qi-Ming Tan

Jie Zhang

Gong-Hao Li

Yun-Feng Zhao

TRPC6 Channel Regulates Airway Remodeling in Chronic Obstructive Pulmonary Disease Causing Right Heart Failure

TRPC6通道调控慢性阻塞性肺疾病引起的右心衰竭中的气道重塑

Seed germination and seedling establishment are characterized by changes in the intracellular redox state modulated by accelerated production of nitric oxide (NO) and reactive oxygen species (ROS). Redox regulation and enhanced accumulation of NO and ROS, approaching excessively high levels during seed imbibition, are critically important for breaking endodormancy and inducing germination.

Natalia V. Bykova

Abir U. Igamberdiev

Redox Control of Seed Germination is Mediated by the Crosstalk of Nitric Oxide and Reactive Oxygen Species

氧化还原控制种子萌发的机制受一氧化氮与活性氧相互作用的影响

Diabetic nephropathy (DN) is a major cause of end-stage renal disease, with no therapeutic interventions available to control its progression. Ferroptosis, an iron-dependent regulated cell death characterized by lipid peroxidation, plays a pivotal role in the pathogenesis of DN. Human umbilical cord mesenchymal stem cells (hUCMSCs) are an effective treatment modality for DN; however, the underlying mechanism of action remains unclear. The aim of the present study was to investigate whether hUCMSCs alleviate DN via inhibiting ferroptosis and its molecular mechanisms in type 2 diabetic mice and high-glucose and palmitate-stimulated human renal tubular epithelial cell (HK-11) models.

Yuexin Zhu

Changqing Dong

Zhiheng Xu

Yan Lou

Na Tian

Yucan Guan

Ping Nie

Manyu Luo

Ping Luo

Human Umbilical Cord Mesenchymal Stem Cells Alleviate Diabetic Nephropathy by Inhibiting Ferroptosis via the JNK/KEAP1/NRF2 Signaling Pathway

人脐带间充质干细胞通过抑制JNK/KEAP1/NRF2信号通路减轻糖尿病肾病中的铁死亡

Abbreviation	Antioxid. Redox Signal.
Journal Impact	6.10
Quartiles(Global)	ENDOCRINOLOGY & METABOLISM(Q1)

ISSN	1523-0864, 1557-7716
h-index	230

Publication Information	Publisher: Mary Ann Liebert Inc.，Publishing cycle: Semimonthly，Journal Type: journal，Open Access Journals: No
Basic data	Year of publication: 1999，Proportion of original research papers: 89.26%，Self Citation Rate:3.40%， Gold OA Rate: 11.43%
Average review cycle	网友分享经验：一般,3-6周
Average recruitment ratio	网友分享经验：较难

Antioxidants and Redox Signaling

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Forkhead Homeobox Type O Transcription Factors in the Responses to Oxidative Stress

Butyrate-stimulated H₂S Production in Colon Cancer Cells

Redox Regulation of Multidrug Resistance in Cancer Chemotherapy: Molecular Mechanisms and Therapeutic Opportunities

Dynamic Regulation of Ferroptosis by Lipid Metabolism

The Emerging Roles of Hydrogen Sulfide in Ferroptosis

Alterations in Mitochondrial Function in Pulmonary Vascular Diseases

Anti-Inflammatory Effects of Hydrogen Sulfide in Axes Between Gut and Other Organs

TRPC6 Channel Regulates Airway Remodeling in Chronic Obstructive Pulmonary Disease Causing Right Heart Failure

Redox Control of Seed Germination is Mediated by the Crosstalk of Nitric Oxide and Reactive Oxygen Species

Human Umbilical Cord Mesenchymal Stem Cells Alleviate Diabetic Nephropathy by Inhibiting Ferroptosis via the JNK/KEAP1/NRF2 Signaling Pathway

Antioxidants and Redox Signaling

Journal Citation Format

A journal article with 1 author

A journal article with 2 authors

A journal article with 3 authors

A journal article with 5 or more authors

Books Citation Format

Thesis Citation Format

Web sites Citation Format

Patent Citation Format

Staying up late manually editing references? ivySCI automatically matches journals and helps you generate references with a single click.

Share Submission Experience

Forkhead Homeobox Type O Transcription Factors in the Responses to Oxidative Stress

Butyrate-stimulated H2S Production in Colon Cancer Cells

Redox Regulation of Multidrug Resistance in Cancer Chemotherapy: Molecular Mechanisms and Therapeutic Opportunities

Dynamic Regulation of Ferroptosis by Lipid Metabolism

The Emerging Roles of Hydrogen Sulfide in Ferroptosis

Alterations in Mitochondrial Function in Pulmonary Vascular Diseases

Anti-Inflammatory Effects of Hydrogen Sulfide in Axes Between Gut and Other Organs

TRPC6 Channel Regulates Airway Remodeling in Chronic Obstructive Pulmonary Disease Causing Right Heart Failure

Redox Control of Seed Germination is Mediated by the Crosstalk of Nitric Oxide and Reactive Oxygen Species

Human Umbilical Cord Mesenchymal Stem Cells Alleviate Diabetic Nephropathy by Inhibiting Ferroptosis via the JNK/KEAP1/NRF2 Signaling Pathway

Butyrate-stimulated H₂S Production in Colon Cancer Cells