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| 1 | Research trends, hot spots and prospects for necroptosis in the field of neuroscience显示文摘There are two types of cell death-apoptosis and necrosis. Apoptosis is cell death regulated by cell signaling pathways, while necrosis has until recently been considered a passive mechanism of cell death caused by environmental pressures. However, recent studies show that necrosis can also be regulated by specific cell signaling pathways. This mode of death, termed necroptosis, has been found to be related to the occurrence and development of many diseases. We used bibliometrics to analyze the global output of literature on necroptosis in the field of neuroscience published in the period 2007–2019 to identify research hotspots and prospects. We included 145 necroptosisrelated publications and 2239 references published in the Web of Science during 2007–2019. Visualization analysis revealed that the number of publications related to necroptosis has increased year by year, reaching a peak in 2019. China is the country with the largest number of publications. Key word and literature analyses demonstrated that mitochondrial function change, stroke, ischemia/reperfusion and neuroinflammation are likely the research hotspots and future directions of necroptosis research in the nervous system. The relationship between immune response-related factors, damage-associated molecular patterns, pathogen-associated molecular patterns and necroptosis may become a potential research hotspot in the future. Taken together, our findings suggest that although the inherent limitations of bibliometrics may affect the accuracy of the literature-based prediction of research hotspots, the results obtained from the included publications can provide a reference for the study of necroptosis in the field of neuroscience. | Wei-Tao Yan Shuang Lu Yan-Di Yang Wen-Ya Ning Yan Cai Xi-Min Hu Qi Zhang Kun Xiong | 2021 | Neural Regeneration Research2021，16，8： | 7 |
| 2 | Regulatory role of calpain in neuronal death显示文摘Calpains are a group of calcium-dependent proteases that are over activated by increased intracellular calcium levels under pathological conditions. A wide range of substrates that regulate necrotic, apoptotic and autophagic pathways are affected by calpain. Calpain plays a very important role in neuronal death and various neurological disorders. This review introduces recent research progress related to the regulatory mechanisms of calpain in neuronal death. Various neuronal programmed death pathways including apoptosis, autophagy and regulated necrosis can be divided into receptor interacting protein-dependent necroptosis, mitochondrial permeability transition-dependent necrosis, pyroptosis and poly(ADP-ribose)polymerase 1-mediated parthanatos. Calpains cleave series of key substrates that may lead to cell death or participate in cell death. Regarding the investigation of calpain-mediated programed cell death, it is necessary to identify specific inhibitors that inhibit calpain mediated neuronal death and nervous system diseases. | Si-ying Cheng Shu-chao Wang Ming Lei Zhen Wang Kun Xiong | 2018 | Neural Regeneration Research2018，13，3： | 6 |
| 3 | RIP3/MLKL-mediated neuronal necroptosis induced by methamphetamine at 39℃显示文摘Methamphetamine is one of the most prevalent drugs abused in the world.Methamphetamine abusers usually present with hyperpyrexia (39℃),hallucination and other psychiatric symptoms.However,the detailed mechanism underlying its neurotoxic action remains elusive.This study investigated the effects of methamphetamine + 39℃ on primary cortical neurons from the cortex of embryonic Sprague-Dawley rats.Primary cortex neurons were exposed to 1 mM methamphetamine + 39℃.Propidium iodide staining and lactate dehydrogenase release detection showed that methamphetamine + 39℃ triggered obvious necrosis-like death in cultured primary cortical neurons,which could be partially inhibited by receptor-interacting protein-1 (RIP1) inhibitor Necrostatin-1 partially.Western blot assay results showed that there were increases in the expressions of receptor-interacting protein-3 (RIP3) and mixed lineage kinase domain-like protein (MLKL) in the primary cortical neurons treated with 1 mM methamphetamine + 39℃ for 3 hours.After pre-treatment with RIP3 inhibitor GSK’872,propidium iodide staining and lactate dehydrogenase release detection showed that neuronal necrosis rate was significantly decreased;RIP3 and MLKL protein expression significantly decreased.Immunohistochemistry staining results also showed that the expressions of RIP3 and MLKL were up-regulated in brain specimens from humans who had died of methamphetamine abuse.Taken together,the above results suggest that methamphetamine + 39℃ can induce RIP3/MLKL regulated necroptosis,thereby resulting in neurotoxicity.The study protocol was approved by the Medical Ethics Committee of the Third Xiangya Hospital of Central South University,China (approval numbers: 2017-S026 and 2017-S033) on March 7,2017. | Li-Min Guo Zhen Wang Shi-Ping Li Mi Wang Wei-Tao Yan Feng-Xia Liu Chu-Dong Wang Xu-Dong Zhang Dan Chen Jie Yan Kun Xiong | 2020 | Neural Regeneration Research2020，15，5： | 5 |
| 4 | Mixed lineage kinase domain-like protein induces RGC-5 necroptosis following elevated hydrostatic pressure显示文摘 | Lvshuang Liao Lei Shang Na Li Shuchao Wang Mi Wang Yanxia Huang Dan Chen Jufang Huang Kun Xiong | 2017 | Acta Biochimica et Biophysica Sinica2017，49，10： | 5 |
| 5 | 不同眼压状态下实验性青光眼视网膜神经节细胞p53基因表达显示文摘目的探究不同眼压状态下实验性青光眼视网膜神经节细胞(RGCs)p53基因的表达。方法将经过培养的RGC-5细胞分为对照组、20 mmHg压力组、40 mmHg压力组及60 mmHg压力组,压力组分别施加20、40和60 mmHg的压力,根据分组对培养的RGC-5细胞进行密闭加压处理48 h后,用倒置相差显微镜观察各组细胞的存活状况,用流式细胞仪检测细胞凋亡情况,用半定量反转录聚合酶链反应(RT-PCR)和Western印迹检测p53基因的变化。结果①压力越大,细胞的异常表现越明显;②随着压力的增加,活细胞比例逐渐降低,凋亡和坏死细胞的比例逐渐升高,60 mmHg压力组早期凋亡细胞比例为22.60%,明显高于对照组(9.84%)、20 mmHg压力组(8.18%)、40 mmHg压力组(7.44%),且各组凋亡和坏死细胞比例总体差异存在统计学意义(F=150.8,P<0.001)。③随着压力的增加,p53 mRNA表达逐渐增加,蛋白表达逐渐增加。结论眼压升高会诱导p53 mRNA和蛋白表达增加,从而引发RGCs凋亡和坏死,压力越大,RGCs凋亡和坏死越严重。 | 李素美 王文奇 | 2021 | 中国老年学杂志2021，41，18： | 2 |
| 6 | 青光眼性视网膜神经节细胞程序性坏死的机制显示文摘青光眼是世界第二大致盲性眼病,到2050年,我国青光眼患者将达到2516万,青光眼所导致的社会和经济负担将继续增加[1]。青光眼以视神经损伤和视网膜神经节细胞(retinal ganglion cell,RGC)进行性丧失为主要病理特征,并伴有不可逆的视野缺失和视功能损害。眼压升高、局部缺血、兴奋毒性等因素是青光眼发病的主要原因,但迄今为止尚无医学手段可阻止或逆转青光眼性视神经损害[2]。 | 赵文娟 范春玲 洪俊 何烨 胡熙敏 张齐 熊鲲 | 2021 | 中国医刊2021，56，3： | 2 |
| 7 | Neuroprotective effect of deferoxamine on N-methyI-D-aspartate-induced excitotoxicity in RGC-5 cells显示文摘 | Ying Tian Ye He Weitao Song Endong Zhang Xiaobo Xia | 2017 | Acta Biochimica et Biophysica Sinica2017，49，9： | 1 |
| 8 | 线粒体自噬对缺血性脑卒中的作用及其机制研究进展显示文摘线粒体自噬作为一种选择性自噬,是线粒体质量控制的关键机制之一。脑组织缺血可引发多种分子的级联反应,导致功能障碍线粒体的堆积。线粒体功能障碍可诱导线粒体自噬的激活,通过清除受损或去极化线粒体来维持神经元细胞的稳态。研究表明线粒体自噬与缺血性脑卒中的病理过程密切相关,但其具体机制及其作用一直备受争议。本文就线粒体自噬的发生机制及其在缺血脑组织中的作用进行综述,为临床治疗缺血性脑卒中提供新的思路。 | 李婷婷 王钦鹏 刘晓庆 蔡珂 魏阳阳(综述) 梁成(审校) | 2024 | 中风与神经疾病杂志2024，41，1： | 0 |
| 9 | 坏死性凋亡在眼科的研究进展及其抑制剂的临床应用显示文摘坏死性凋亡是近十几年来细胞死亡领域的重大发现。目前在眼科领域,已经从角膜疾病、青光眼、视网膜疾病等方向发现了坏死性凋亡通路的激活。除了针对受体相互作用蛋白1(RIP1)靶点的Necrostatin-1(Nec-1)坏死性凋亡抑制剂之外,受体相互作用蛋白3(RIP3)抑制剂GSK2399872A(GSK872)和针对混合谱系激酶结构域样蛋白(MLKL)靶点的新型抑制剂TC13172等药物在细胞死亡机制方面取得了重大突破。目前,坏死性凋亡抑制剂已经在眼科的多种疾病模型中证明了其保护作用。本文重点概述了坏死性凋亡的分子机制及其抑制剂在眼科中的研究成果,探讨坏死性凋亡作为眼科疾病治疗新靶点的潜力,并对其在眼科领域的进一步研究提出建议。 | 颜鑫霖 李轩 | 2023 | 实用医学杂志2023，39，17： | 0 |
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