Research hotspots and trends of multimodality MRI on vascular cognitive impairment in recent 12 years: A bibliometric analysis.

BACKGROUND: Multimodality magnetic resonance imaging (MRI) is widely used to detect vascular cognitive impairment (VCI). However, a bibliometric analysis of this issue remains unknown. Therefore, this study aimed to explore the research hotspots and trends of multimodality MRI on VCI over the past 12 years based on the Web of Science core collection using CiteSpace Software (6.1R2). METHODS: Literature related to multimodality MRI for VCI from 2010 to 2021 was identified and analyzed from the Web of Science core collection database. We analyzed the countries, institutions, authors, cited journals, references, keyword bursts, and clusters using CiteSpace. RESULTS: In total, 587 peer-reviewed documents were retrieved, and the annual number of publications showed an exponential growth trend over the past 12 years. The most productive country was the USA, with 182 articles, followed by China with 134 papers. The top 3 active academic institutions were Capital Medical University, Radboud UNIV Nijmegen, and UNIV Toronto. The most productive journal was the Journal of Alzheimer's Disease (33 articles). The most co-cited journal was Neurology, with the highest citations (492) and the highest intermediary centrality (0.14). The top-ranked publishing author was De Leeuw FE (17 articles) with the highest intermediary centrality of 0.04. Ward Law JM was the most cited author (123 citations) and Salat Dh was the most centrally cited author (0.24). The research hotspots of multimodal MRI for VCI include Alzheimer disease, vascular cognitive impairment, white matter intensity, cerebrovascular disease, dementia, mild cognitive impairment, neurovascular coupling, acute ischemic stroke, depression, and cerebral ischemic stroke. The main frontiers in the keywords are fMRI, vascular coupling, and cerebral ischemic stroke, and current research trends include impact, decline, and classification. CONCLUSIONS: The findings from this bibliometric study provide research hotspots and trends for multimodality MRI for VCI over the past 12 years, which may help researchers identify hotspots and explore cutting-edge trends in this field.

p62 Suppressed VK3-induced Oxidative Damage Through Keap1/Nrf2 Pathway In Human Ovarian Cancer Cells.

Imbalance of redox homeostasis may be responsible for the resistance of cancer to chemotherapy. Currently, increasing studies demonstrated that vitamin K3 (VK3), which promoted the production of ROS, had potential to be developed as an anti-tumor agent. We found SKOV3/DDP cells with high levels of p62 were insensitive to VK3 compared with SKOV3 cells. Furthermore, Nrf2 downstream antioxidant genes such as HO-1(heme oxygenase 1) and NQO1 (NAD (P) H: quinone oxidoreductase 1) were upregulated in SKOV3/DDP cells with VK3 treatment, which indicated VK3 activated Nrf2 signaling in SKOV3/DDP cells. Moreover, co-localization of p62 and Keap1 was also observed. Suppression of p62 expression increased the apoptosis induced by VK3, and the expression of Nrf2, HO-1 and NQO1 were all downregulated in SKOV3/DDP cells. Our results suggested that overexpressed p62 may protect cells from oxidative damage caused by VK3 through activating Keap1/Nrf2 signaling in ovarian cancer.

Bcl-2 family proteins are involved in the signal crosstalk between endoplasmic reticulum stress and mitochondrial dysfunction in tumor chemotherapy resistance.

Tumor cells overexpress antiapoptotic proteins of the Bcl-2 (B-cell leukemia/lymphoma-2) family, which can lead to both escape from cell death and resistance to chemotherapeutic drugs. Recent studies suggest that the endoplasmic reticulum (ER) can produce proapoptotic signals, amplifying the apoptotic signaling cascade. The crosstalk between mitochondria and ER plays a decisive role in many cellular events but especially in cell death. Bcl-2 family proteins located in the ER and mitochondria can influence not only the function of the two organelles but also the interaction between them. Therefore, the Bcl-2 family of proteins may also be involved in the mechanism of tumor chemotherapy resistance by influencing crosstalk between the ER and mitochondria. In this review we will briefly discuss evidence to support this concept.