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Platelet therapy:A novel strategy for liver regeneration,anti-fibrosis,and anti-apoptosis
Platelet therapy:A novel strategy for liver regeneration,anti-fibrosis,and anti-apoptosis
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摘要：
Platelets contain bio-physiological substances,including insulin-like growth factor-1,vascular endothelial growth factor,platelet-derived growth factor,hepatocyte growth factor,serotonin,transforming growth factor-β,adenosine diphosphate,adenosine tri-phosphate,and epidermal growth factor.Platelets have conventionally been considered to exacerbate the inflammatory response and liver injury.Recently,platelets were discovered to have a positive impact on the liver.In this review,we present experimental and clinical evidence indicating that platelets accelerate liver regeneration and have anti-fibrosis and antiapoptosis activity,and we detail the mechanisms of action.Platelets accelerate liver regeneration by three different mechanisms:(1)a direct effect on hepatocytes,(2)a cooperative effect with liver sinusoidal endothelial cells,and(3)a collaborative effect with Kupffer cells.Platelets exert anti-fibrotic activity by deactivating hepatic stellate cells via the adenosinecyclic adenosine 5’-monophosphate signaling pathway.Platelets prevent hepatocyte apoptosis by activating the Akt pathway and up-regulating Bcl-xL,which suppresses caspase-3 activation.Platelet therapy with thrombopoietin,thrombopoietin receptor agonists,and platelet transfusion has the advantages of convenience and cost-efficiency over other treatments.We propose that in the future,platelet therapy will play a promising role in the treatment of the various liver disorders that currently challenge the surgical field,such as liver failure after a massive hepatectomy,hepatectomy of a cirrhotic liver,and small grafts in liver transplantation.
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研究主题发展历程
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PLATELET
THERAPY
LIVER
regeneration
LIVER
fibrosis
HEPATOCYTE
apoptosis
Growth
factor
研究起点
研究来源
研究分支
研究去脉
引文网络交叉学科
相关学者/机构
期刊影响力
世界外科手术杂志
主办单位：
百世登出版集团有限公司
出版周期：
不定期
ISSN：
2219-2832
CN：
开本：
出版地：
北京市朝阳区东四环中路62号楼远洋国际中
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出版文献量（篇）
61
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0
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0
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