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作 者:张帆[1] 张聪聪[1] 张海波[1] ZHANG Fan;ZHANG Cong-cong;ZHANG Hai-bo(Department of Cardiac Surgery,Beijing Anzhen Hospital.Capital Medical University,Beijing 100029,China)
机构地区:[1]首都医科大学附属北京安贞医院心外科,北京市100029
出 处:《中国心血管病研究》2020年第4期325-329,共5页Chinese Journal of Cardiovascular Research
基 金:国家自然科学基金(81871758)。
摘 要:主动脉瓣钙化性狭窄是一种常见的引发主要不良心血管事件的心血管疾病,但目前尚无有效的医疗干预手段来延迟或阻止其进展.心脏代谢风险因素(包括吸烟和男性等)与主动脉瓣狭窄有关.近年的研究也明确了免疫和炎症反应(包括氧化脂质、各种细胞因子和生物矿化)对主动脉瓣钙化的重要调节作用.炎症和代谢通过调节骨形成相关的信号通路参与心血管系统中骨生成进而导致血管钙化.随着研究的深入,主动脉瓣钙化性疾病(CAVD)不再被认为是一种在高龄时发生的单纯的钙沉积被动过程,而是一个涉及瓣膜、循环、骨髓来源的细胞、巨噬细胞异质性以及遗传、生化和机械等因素的复杂调控过程.本综述主要讨论最近发现的促进CAVD的炎症和脂质代谢的危险因素在主动脉瓣钙化形成机制的研究进展,为未来发展抑制CAVD进展的治疗策略提供理论基础.Aortic valve calcification stenosis is a common cardiovascular disease that causes major adverse cardiovascular events.But there is no effective medical intervention to delay or prevent its progression to date.Cardiac metabolic risk factors(including smoking and men)are associated with aortic valve stenosis.Recent studies have also identified important regulatory effects of immune and inflammatory responses(including oxidized lipids.various cytokines and biomineralization)on aortic valve calcification.Inflammation and metabolism participate in osteogenesis in the cardiovascular system by regulating signaling pathways related to bone formation,which leads to vascular calcification.With the deepening of research,calcific aortic valve disease(CAVD)is no longer considered as a passive calcium deposition process that occurs at old age,but a complex regulatory network associated with valve,circulation,bone marrow-derived cells,macrophages heterogeneity and other biochemical and mechanical factors.This review aims to discusses the recent advances in research on the molecular mechanisms of inflammation and lipids metabolic risk factors in aortic valve calcification to provide a theoretical basis for future development of CAVD treatment strategies.
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