{"title":"肝窦状内皮细胞:肝纤维化中一个重要却常被忽视的角色","authors":"Jiaorong Qu, Le Wang, Yufei Li, Xiaojiaoyang Li","doi":"10.3350/cmh.2024.0022","DOIUrl":null,"url":null,"abstract":"<p><p>Liver sinusoidal endothelial cells (LSECs) are liver-specific endothelial cells with the highest permeability than other mammalian endothelial cells, characterized by the presence of fenestrae on their surface, the absence of diaphragms and the lack of basement membrane. Located at the interface between blood and other liver cell types, LSECs mediate the exchange of substances between the blood and the Disse space, playing a crucial role in maintaining substance circulation and homeostasis of multicellular communication. As the initial responders to chronic liver injury, the abnormal LSEC activation not only changes their own physicochemical properties but also interrupts their communication with hepatic stellate cells and hepatocytes, which collectively aggravates the process of liver fibrosis. In this review, we have comprehensively updated the various pathways by which LSECs were involved in the initiation and aggravation of liver fibrosis, including but not limited to cellular phenotypic change, the induction of capillarization, decreased permeability and regulation of intercellular communications. Additionally, the intervention effects and latest regulatory mechanisms of anti-fibrotic drugs involved in each aspect have been summarized and discussed systematically. As we studied deeper into unraveling the intricate role of LSECs in the pathophysiology of liver fibrosis, we unveil a promising horizon that pave the way for enhanced patient outcomes.</p>","PeriodicalId":10275,"journal":{"name":"Clinical and Molecular Hepatology","volume":null,"pages":null},"PeriodicalIF":14.0000,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11261236/pdf/","citationCount":"0","resultStr":"{\"title\":\"Liver sinusoidal endothelial cell: An important yet often overlooked player in the liver fibrosis.\",\"authors\":\"Jiaorong Qu, Le Wang, Yufei Li, Xiaojiaoyang Li\",\"doi\":\"10.3350/cmh.2024.0022\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Liver sinusoidal endothelial cells (LSECs) are liver-specific endothelial cells with the highest permeability than other mammalian endothelial cells, characterized by the presence of fenestrae on their surface, the absence of diaphragms and the lack of basement membrane. Located at the interface between blood and other liver cell types, LSECs mediate the exchange of substances between the blood and the Disse space, playing a crucial role in maintaining substance circulation and homeostasis of multicellular communication. As the initial responders to chronic liver injury, the abnormal LSEC activation not only changes their own physicochemical properties but also interrupts their communication with hepatic stellate cells and hepatocytes, which collectively aggravates the process of liver fibrosis. In this review, we have comprehensively updated the various pathways by which LSECs were involved in the initiation and aggravation of liver fibrosis, including but not limited to cellular phenotypic change, the induction of capillarization, decreased permeability and regulation of intercellular communications. Additionally, the intervention effects and latest regulatory mechanisms of anti-fibrotic drugs involved in each aspect have been summarized and discussed systematically. As we studied deeper into unraveling the intricate role of LSECs in the pathophysiology of liver fibrosis, we unveil a promising horizon that pave the way for enhanced patient outcomes.</p>\",\"PeriodicalId\":10275,\"journal\":{\"name\":\"Clinical and Molecular Hepatology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":14.0000,\"publicationDate\":\"2024-07-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11261236/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Clinical and Molecular Hepatology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.3350/cmh.2024.0022\",\"RegionNum\":1,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/2/28 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q1\",\"JCRName\":\"GASTROENTEROLOGY & HEPATOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical and Molecular Hepatology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.3350/cmh.2024.0022","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/2/28 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"GASTROENTEROLOGY & HEPATOLOGY","Score":null,"Total":0}
引用次数: 0
摘要
肝窦状内皮细胞(LSECs)是肝脏特异性内皮细胞,与其他哺乳动物内皮细胞相比,其通透性最高,其特点是表面有栅栏、无隔膜、无基底膜。LSECs 位于血液和其他类型肝细胞之间的界面,介导血液和 Disse 空间之间的物质交换,在维持物质循环和多细胞通讯平衡方面发挥着至关重要的作用。作为慢性肝损伤的最初反应者,LSECs的异常活化不仅改变了其自身的理化性质,还中断了其与造血干细胞和肝细胞的交流,共同加剧了肝纤维化的进程。在这篇综述中,我们全面更新了 LSECs 参与肝纤维化启动和进展的各种途径,包括但不限于细胞表型改变、毛细血管化诱导、通透性降低和细胞间通讯调控。此外,还系统地总结和讨论了各方面所涉及的抗纤维化药物的干预效果和最新调控机制。随着我们深入研究揭示 LSECs 在肝纤维化病理生理学中错综复杂的作用,我们将揭开一个充满希望的前景,为改善患者预后铺平道路。
Liver sinusoidal endothelial cell: An important yet often overlooked player in the liver fibrosis.
Liver sinusoidal endothelial cells (LSECs) are liver-specific endothelial cells with the highest permeability than other mammalian endothelial cells, characterized by the presence of fenestrae on their surface, the absence of diaphragms and the lack of basement membrane. Located at the interface between blood and other liver cell types, LSECs mediate the exchange of substances between the blood and the Disse space, playing a crucial role in maintaining substance circulation and homeostasis of multicellular communication. As the initial responders to chronic liver injury, the abnormal LSEC activation not only changes their own physicochemical properties but also interrupts their communication with hepatic stellate cells and hepatocytes, which collectively aggravates the process of liver fibrosis. In this review, we have comprehensively updated the various pathways by which LSECs were involved in the initiation and aggravation of liver fibrosis, including but not limited to cellular phenotypic change, the induction of capillarization, decreased permeability and regulation of intercellular communications. Additionally, the intervention effects and latest regulatory mechanisms of anti-fibrotic drugs involved in each aspect have been summarized and discussed systematically. As we studied deeper into unraveling the intricate role of LSECs in the pathophysiology of liver fibrosis, we unveil a promising horizon that pave the way for enhanced patient outcomes.
期刊介绍:
Clinical and Molecular Hepatology is an internationally recognized, peer-reviewed, open-access journal published quarterly in English. Its mission is to disseminate cutting-edge knowledge, trends, and insights into hepatobiliary diseases, fostering an inclusive academic platform for robust debate and discussion among clinical practitioners, translational researchers, and basic scientists. With a multidisciplinary approach, the journal strives to enhance public health, particularly in the resource-limited Asia-Pacific region, which faces significant challenges such as high prevalence of B viral infection and hepatocellular carcinoma. Furthermore, Clinical and Molecular Hepatology prioritizes epidemiological studies of hepatobiliary diseases across diverse regions including East Asia, North Asia, Southeast Asia, Central Asia, South Asia, Southwest Asia, Pacific, Africa, Central Europe, Eastern Europe, Central America, and South America.
The journal publishes a wide range of content, including original research papers, meta-analyses, letters to the editor, case reports, reviews, guidelines, editorials, and liver images and pathology, encompassing all facets of hepatology.