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作 者:陈梦琪 刘婷婷 孙芳玲 田欣 郑文荣 祝自新 王宇峰 马连素 王文 CHEN Mengqi;LIU Tingting;SUN Fangling;TIAN Xin;ZHENG Wenrong;ZHU Zixin;WANG Yufeng;MA Liansu;WANG Wen(Department of Experimental Animal Laboratory,Xuanwu Hospital of Capital Medical University,Beijing 100053,China;Beijing Geriatric Medical Research Center,Beijing 100053;Beijing Medical Health Technology Development Center,Beijing 100101;Beijing Institute for Brain Disorders,Beijing 100069)
机构地区:[1]首都医科大学宣武医院实验动物室,北京100053 [2]北京市老年病医疗研究中心,北京100053 [3]北京医药健康科技发展中心,北京100101 [4]北京市脑重大疾病研究院,北京100069
出 处:《中国比较医学杂志》2024年第2期144-153,共10页Chinese Journal of Comparative Medicine
基 金:国家自然科学基金(82173795)。
摘 要:心血管疾病是一种危害人类健康的疾病,心肌梗死导致的收缩性心力衰竭是造成死亡的主要原因。既往观点认为,成年哺乳动物心脏中心肌细胞自我增殖更新能力有限,而近年来大量报道指出,哺乳动物在出生早期具备心肌再生的能力,并且其强度足以修复受损的心脏组织。新生鼠心肌再生现象的发现,为探讨影响心肌再生的相关机制提供了理想的动物模型,继而许多能够逆转心肌细胞周期阻滞和促进心肌再生的调控机制得以揭示。本文基于近几年开展的有关新生鼠心肌再生的研究,综述了影响心肌再生基因表达的因素(ncRNAs、转录因子等)、心肌再生相关信号通路和非心肌细胞(细胞外基质、免疫反应、心外膜等)对心肌再生的调节作用,以期为实现成年哺乳动物心肌损伤后心肌再生提供方向。Cardiovascular disease is a health hazard to humans and systolic heart failure due to myocardial infarction is a major cause of death.It was previously thought that myocardial cells of the adult mammalian heart possess a limited ability to proliferate and self⁃renew.However,it has been widely reported that mammals have the ability to regenerate the myocardium,which is restricted to early postnatal life,and that it is strong enough to repair damaged heart tissue.The discovery of myocardial regeneration in neonatal hearts has provided an ideal animal model to investigate the mechanisms that affect myocardial regeneration,and many mechanisms that reverse myocardial cell cycle arrest and promote myocardial regeneration have been revealed.In this article,we review the factors affecting gene expression for myocardial regeneration(e.g.,ncRNAs and transcription factors),myocardial regeneration⁃related signaling pathways,and the regulation of myocardial regeneration by non⁃myocardial cells(e.g.,extracellular matrix,immune response,and epicardium)to provide directions for achieving myocardial regeneration after myocardial injury in adult mammals.
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