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血小板结合蛋白:血栓性疾病的一个潜在治疗靶点。

Podoplanin: A potential therapeutic target for thrombotic diseases.

作者信息

Huang Yaqian, Lu Manli, Wang Yi, Zhang Chunyuan, Cao Yongjun, Zhang Xia

机构信息

Department of Neurology, Clinical Research Center of Neurological Disease, The Second Affiliated Hospital of Soochow University, Suzhou, China.

Department of Rehabilitation, The Second Affiliated Hospital of Soochow University, Suzhou, China.

出版信息

Front Neurol. 2023 Mar 9;14:1118843. doi: 10.3389/fneur.2023.1118843. eCollection 2023.

DOI:10.3389/fneur.2023.1118843
PMID:36970507
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10033871/
Abstract

As a specific lymphatic marker and a key ligand of C-type lectin-like receptor 2 (CLEC-2), podoplanin (Pdpn) is involved in various physiological and pathological processes such as growth and development, respiration, blood coagulation, lymphangiogenesis, angiogenesis, and inflammation. Thrombotic diseases constitute a major cause of disability and mortality in adults, in which thrombosis and inflammation play a crucial role. Recently, increasing evidence demonstrates the distribution and function of this glycoprotein in thrombotic diseases such as atherosclerosis, ischemic stroke, venous thrombosis, ischemic-reperfusion injury (IRI) of kidney and liver, and myocardial infarction. Evidence showed that after ischemia, Pdpn can be acquired over time by a heterogeneous cell population, which may not express Pdpn in normal conditions. In this review, the research progresses in understanding the roles and mechanisms of podoplanin in thromobotic diseases are summarized. The challenges of podoplanin-targeted approaches for disease prognosis and preventions are also discussed.

摘要

作为一种特定的淋巴管标志物和C型凝集素样受体2(CLEC-2)的关键配体,血小板内皮细胞黏附分子(Pdpn)参与多种生理和病理过程,如生长发育、呼吸、血液凝固、淋巴管生成、血管生成和炎症。血栓性疾病是成年人致残和死亡的主要原因,其中血栓形成和炎症起着至关重要的作用。最近,越来越多的证据表明这种糖蛋白在动脉粥样硬化、缺血性中风、静脉血栓形成、肝肾缺血再灌注损伤(IRI)和心肌梗死等血栓性疾病中的分布和功能。有证据表明,缺血后,Pdpn可随时间被一群异质性细胞获得,这些细胞在正常情况下可能不表达Pdpn。在这篇综述中,总结了在理解血小板内皮细胞黏附分子在血栓性疾病中的作用和机制方面的研究进展。还讨论了以血小板内皮细胞黏附分子为靶点的疾病预后和预防方法所面临的挑战。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae37/10033871/aaed642de3a8/fneur-14-1118843-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae37/10033871/aaed642de3a8/fneur-14-1118843-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae37/10033871/aaed642de3a8/fneur-14-1118843-g0001.jpg

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本文引用的文献

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Foudroyant cerebral venous (sinus) thrombosis triggered through CLEC-2 and GPIIb/IIIa dependent platelet activation.通过CLEC-2和糖蛋白IIb/IIIa依赖性血小板激活引发的暴发性脑静脉(窦)血栓形成。
Nat Cardiovasc Res. 2022 Feb;1(2):132-141. doi: 10.1038/s44161-021-00017-1. Epub 2022 Feb 10.
2
Transcriptome sequencing analysis revealed the molecular mechanism of podoplanin neutralization inhibiting ischemia/reperfusion-induced microglial activation.转录组测序分析揭示了血小板反应蛋白-1中和作用抑制缺血/再灌注诱导的小胶质细胞激活的分子机制。
Ann Transl Med. 2022 Jun;10(11):638. doi: 10.21037/atm-22-1952.
3
The Role of Podoplanin in the Immune System and Inflammation.
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J Inflamm Res. 2022 Jun 17;15:3561-3572. doi: 10.2147/JIR.S366620. eCollection 2022.
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CLEC-2-dependent platelet subendothelial accumulation by flow disturbance contributes to atherogenesis in mice.血流紊乱导致 CLEC-2 依赖性血小板在下皮细胞中的堆积,从而促进了小鼠的动脉粥样硬化形成。
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