Research trends, hot spots and prospects for necroptosis in the field of neuroscience.

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 necroptosis-related 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.

Citation

Wei-Tao Yan, Shuang Lu, Yan-Di Yang, Wen-Ya Ning, Yan Cai, Xi-Min Hu, Qi Zhang, Kun Xiong. Research trends, hot spots and prospects for necroptosis in the field of neuroscience. Neural regeneration research. 2021 Aug;16(8):1628-1637

PMID: 33433494

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