刊·见 | Free Radical Research详探人体内的“无敌破坏王” —— 自由基

根据Scopus显示, Free Radical Research的

CiteScore(2022)为7.2

CiteScoreTracker(2023)为6.7

在生物化学、遗传学和分子生物学:生物化学领域排名136/428

作者须知

收稿文章类型

Research papers

Hypotheses

Reviews

审稿周期

从提交稿件到获取初审意见,平均需要11天

获取首个同行评审决定,平均需要32天

稿件接收后,在线出版平均需要12天

编辑团队

Free Radical Research的主编由内田浩二(日本东京大学农业与生命科学研究生院)担任。副主编团队由8名研究人员组成,期刊编委会汇集了来自美国、中国、日本等地的行业翘楚。

主编介绍

内田浩二

内田浩二是东京大学农业与生命科学研究生院应用生物化学系食品化学实验室教授。他的跨学科研究领域包括食品科学、脂质过氧化、天然抗体和先天免疫。

作者分布

根据JCR显示,近三年在Free Radical Research发文的国家中,发文排名前三的是:

中国

日本

印度

近三年,在Free Radical Research发文的全球高校和科研机构中,发文排名前三的是:

日本九州大学

日本名古屋大学

日本量子科学与技术研究所

近三年刊内高被引文章

铁蛋白沉积与心血管疾病:自由基诱导脂质过氧化的作用

作者:Xin Chen et al.

文章摘要:

Cardiovascular disease (CVD), including heart attack, stroke, heart failure, arrhythmia, and other congenital heart diseases remain the leading cause of morbidity and mortality worldwide. The leading cause of deaths in CVD is attributed to myocardial infarction due to the rupture of atherosclerotic plaque. Atherosclerosis refers a condition when restricted or even blockage of blood flow occurs due to the narrowing of blood vessels as a result of the buildup of plaques composed of oxidized lipids. It is well-established that free radical oxidation of polyunsaturated fatty acids (PUFAs) in lipoproteins or cell membranes, termed lipid peroxidation (LPO), plays a significant role in atherosclerosis. LPO products are involved in immune responses and cell deaths in this process, in which previous evidence supports the role of programmed cell death (apoptosis) and necrosis. Ferroptosis is a newly identified form of regulated cell death characterized by the iron-dependent accumulation of lipid hydroperoxides to lethal levels, which exhibits distinct features from apoptosis, necrosis and autophagy in morphology, biochemistry and genetics. Emerging evidence appears to demonstrate that ferroptosis is also involved in CVD. In this review, we summarize the recent progress on ferroptosis in CVD and atherosclerosis, highlighting the role of free radical LPO. The evidence underlying the ferroptosis and challenges in the field will also be critically discussed.

MicroRNA-670-3p通过靶向ACSL4抑制人胶质母细胞瘤细胞的铁变态反应

作者:Chong Bao et al.

文章摘要:

Glioblastoma is one of the most frequent malignant tumors derived from the brain in adults with very poor prognosis. Ferroptosis is implicated in the initiation and progression of various tumors, including the glioblastoma. The present study aims to investigate the function of microRNA (miR)-670-3p in glioblastoma, and tries to demonstrate whether ferroptosis is involved in this process. Human glioblastoma cell lines, U87MG and A172, were transfected with the inhibitor, mimic and matched negative controls of miR-670-3p to manipulate intracellular miR-670-3p level. To validate the involvement of ferroptosis in miR-670-3p inhibitor-mediated tumor suppressive effects, ferrostain-1 and liproxstatin-1 were used to inhibit ferroptosis in the presence of miR-670-3p inhibitor. In addition, the small interfering RNA against acyl-CoA synthase long chain family member 4 (ACSL4) was used to knock down endogenous ACSL4 expression. To validate the combined effects between miR-670-3p inhibitor and temozolomide (TMZ), cells were pretreated with TMZ and then transfected with or without miR-670-3p inhibitor. miR-670-3p level was elevated in human glioblastoma, but decreased upon ferroptotic stimulation. miR-670-3p inhibitor suppressed, while miR-670-3p mimic promoted glioblastoma cell growth through modulating ferroptosis. Mechanistically, ACSL4 was required for the regulation on ferroptosis and growth of glioblastoma cells by miR-670-3p. Moreover, U87MG and A172 cells treated with miR-670-3p inhibitor showed an increased chemosensitivity to TMZ. We prove that miR-670-3p suppresses ferroptosis of human glioblastoma cells through targeting ACSL4, and that inhibiting miR-670-3p can be an alternative, at least adjuvant strategy to treat glioblastoma.

近一年刊内高阅读量文章

用于癌症治疗的低温等离子体的生成和测量:历史回顾

作者:Kenji Ishikawa et al.

Logarithmic diagram of plasmas in density and temperature

文章摘要:

This review provides a description of the historical background of the development of biological applications of low-temperature plasmas. The generation of plasma, methods and devices, plasma sources, and measurements of plasma properties, such as electron dynamics and chemical species generation in both gaseous and aqueous phases, were assessed. Currently, direct irradiation methods for plasma discharges contacting biological surfaces, such as the skin and teeth, are related to plasma biological interactions. Indirect methods using plasma-treated liquids are based on plasma–liquid interactions. The use of these two methods is rapidly increasing in preclinical studies and cancer therapy. The authors address the prospects for further developments in cancer therapeutic applications by understanding the interactions between the plasma and living organisms.

阿萨伊浆果抗氧化保护糖尿病心肌缺血再灌注损伤的分子靶标

作者:Daniela Impellizzeri et al.

Immunohistochemical analysis of iNOS

文章摘要:

Myocardial ischemia/reperfusion injury (MIRI) is the principal cause of death and occurs after prolonged blockage of the coronary arteries. Diabetes represents one of the main factors aggravating myocardial injury. Restoring blood flow is the first intervention against a heart attack, although reperfusion process could cause additional damage, such as the overproduction of reacting oxygen species (ROS). In recent years, açaí berry has gained international attention as a functional food due to its antioxidant and anti-inflammatory properties; not only that but this fruit has shown glucose-lowering effects. Therefore, this study was designed to evaluate the cardioprotective effects of açaí berry on the inflammatory and oxidative responses associated with diabetic MIRI. Diabetes was induced in rats by a single intravenous inoculation of streptozotocin (60 mg/kg) and allowed to develop for 60 days. MIRI was induced by occlusion of the left anterior descending coronary artery for 30 min followed by 2 h of reperfusion. Açaí (200 mg/kg) was administered 5 min before the end of ischemia and 1 h after reperfusion. In this study, we clearly demonstrated that açaí treatment was able to reduce biomarkers of myocardial damage, infarct size, and apoptotic process. Moreover, açaí administrations reduced inflammatory and oxidative response, modulating Nf-kB and Nrf2 pathways. These results suggest that açai berry supplementation could represent a useful strategy for pathological events associated to MIRI.

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