一组来自维也纳医科大学的研究人员发现，某些血小板源生长因子对肝脏的再生过程有主要意义。研究表明，血小板可以促进部分肝切除手术患者中肝组织再生。这也可以作为一个预测潜在的术后问题的起点。相关研究已经发表在《Hepatology》杂志上。
血小板是伤口愈合过程的一个重要组成部分。它们在机体受伤时可以专门分泌关键生长因子，并启动受损组织的再生过程。在最新的研究中，科学家们能够证明α颗粒生长因子的释放与术后肝脏再生密切相关。
早在2014年，这项研究的作者证明，存储于血小板中的5 -羟色胺可以在术后肝再生中发挥关键作用。5 -羟色胺存储在血小板电子致密颗粒(存储细胞器)中，它在激活后可被分泌出。作为血小板活化过程的一部分，第二个类型的α颗粒也被释放了。目前首次证明体内高度选择性释放α颗粒及产生的病理生理后果。
这些颗粒包含刺激和阻碍增长的因素。前几年的体外数据表明，血小板不是存在一个活性或非活性状态，而是它们在一个非常明确的基础上有能力去释放促增长或阻碍增长的因子。在过去时，尚不知道这种机制在体内是否也可以起作用并产生病理生理后果。
肝脏是唯一能够本身再生的器官， 甚至在广泛的损伤或部分被手术切除后(切除)也能再生。高达75%的肝组织被切除后不会带有器官的代谢功能永久受损。
肝脏再生的巨大潜力以及肝脏手术领域的巨大发展意味着肝脏功能受损患者能够接受复杂的重造。然而， 在一定比例的患者手术后肝功能的损伤仍然发生。肝损伤后的并发症严重到可威胁生命，并有相对较高的死亡率。肝衰竭的确切原因目前尚不完全明确。
肝静脉血压可能会选择性α颗粒释放
科学家们现在也已经能够证明血小板源生长因子与肝静脉血压之间有关系。预先存在的肝脏疾病可导致肝静脉血压变化，被认为是术后并发症的危险因素。“我们能够证明，患者的肝静脉血压高，抑制促生长物质释放和阻碍生长因子水平释放的增加。这些发现将有助于我们更好地理解肝静脉血压变化危险的后果。“Starlinger解释道。该研究结果对新的治疗策略旨在确保肝切除手术后改善肝脏再生可能作出重大贡献，因此也可降低肝衰竭的风险，迄今为止肝衰竭仍无法治愈。
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Patrick Starlinger et al. The Profile of Platelet α-Granule Released Molecules Affects Postoperative Liver Regeneration
Patrick Starlinger,Stefanie Haegele,Florian Offensperger,Lukas Oehlberger,David Pereyra, Julia B. Kral,Waltraud C. Schrottmaier,Sigrun Badrnya,Thomas Reiberger,Arnulf Ferlitsch,Judith Stift,Florian Luf,Christine Brostjan,Thomas Gruenberger
Platelets promote liver regeneration via site-specific serotonin release from dense granules, triggering proliferative signaling in hepatocytes. However, the effects of factors derived from platelet α-granules on liver regeneration are unclear, as α-granules contain bioactive molecules with opposing functions. As α-granule molecules are stored in separate compartments, it has been suggested that platelets selectively release their α-granule content dependent on the environmental stimulus. Therefore, we investigated the pattern of circulating α-granule molecules during liver regeneration in 157 patients undergoing partial hepatectomy. We measured plasma levels of α-granule-derived factors in the liver vein at the end of liver resection, as well as on the first postoperative day. We observed a rapid accumulation of platelets within the liver after induction of liver regeneration. Platelet count and P-selectin (a ubiquitous cargo of α-granules) were not associated with postoperative liver dysfunction. However, low plasma levels of vascular endothelial growth factor (VEGF) but high levels of thrombospondin-1 (TSP-1) predicted liver dysfunction after resection. Patients with an unfavorable postoperative α-granule release profile (high TSP-1/low VEGF) showed substantially worse postoperative clinical outcomes. The unfavorable postoperative α-granule release profile was associated with increased postoperative portal venous pressure and von Willebrand factor antigen levels as a marker for intrahepatic endothelial dysfunction. Conclusion: The postoperative profile of circulating platelet-derived factors correlates with the ability of the remnant liver to regenerate. Portal venous pressure and intrahepatic endothelial dysfunction might account for the selective granule release profile. Selective modulation of platelet α-granule release in patients may represent an attractive target for therapeutic interventions to improve liver regeneration and clinical outcomes after partial hepatectomy. This article is protected by copyright. All rights reserved.