血栓形成是一种凝血障碍，是由于凝血、纤溶和免疫因子水平改变而发生的，而这些因子在正常生理条件下可维持止血。在这里，我们回顾了多功能核酶聚（ADP-核糖）聚合酶-1（PARP1）在血栓发病机制中关键基因和细胞过程表达中的直接和间接参与。 PARP1 的生物活性范围包括维持基因组完整性、染色质重塑、碱基切除 DNA 修复、细胞死亡应激反应、血管生成和细胞周期途径。然而，在稳态失衡的情况下，PARP1 活性与癌症、衰老、神经系统疾病和心血管疾病等疾病的发病机制有关。疾病相关的受损细胞利用多种 PARP-1 功能，例如氧化损伤加剧、细胞能量学和凋亡途径、炎症介质的调节、内皮功能障碍的促进以及发病机制中 ERK 介导的信号传导。血栓形成是这样一种发病机制，其包括由于内皮细胞生化改变、血小板活化、粘附分子过度表达、细胞因子释放和白细胞粘附而导致的凝血级联加剧。因此，血栓形成中内皮细胞和炎症细胞的激活暗示了 PARP1 激活在血栓形成中的潜在作用。本文探讨了 PARP1 激活对血栓形成病因的直接影响，并讨论了 PARP1 介导的内皮功能障碍、炎症和疾病表现中的表观遗传调控。了解与血栓形成相关的 PARP1 功能可以阐明新的发病机制，并通过针对 PARP1 活性的新治疗干预措施帮助更好地管理疾病。© 2024。作者获得 Springer Science Business Media, LLC（Springer Nature 旗下子公司）的独家许可。

Thrombosis, a coagulation disorder, occurs due to altered levels of coagulation, fibrinolytic and immune factors, which are otherwise known to maintain hemostasis in normal physiological conditions. Here, we review the direct and indirect participation of a multifunctional nuclear enzyme poly (ADP-ribose) polymerase-1 (PARP1) in the expression of key genes and cellular processes involved in thrombotic pathogenesis. PARP1 biological activities range from maintenance of genomic integrity, chromatin remodeling, base excision DNA repair, stress responses to cell death, angiogenesis and cell cycle pathways. However, under homeostatic imbalances, PARP1 activities are linked with the pathogenesis of diseases, including cancer, aging, neurological disorders, and cardiovascular diseases. Disease-associated distressed cells employ a variety of PARP-1 functions such as oxidative damage exacerbations, cellular energetics and apoptosis pathways, regulation of inflammatory mediators, promotion of endothelial dysfunction, and ERK-mediated signaling in pathogenesis. Thrombosis is one such pathogenesis that comprises exacerbation of coagulation cascade due to biochemical alterations in endothelial cells, platelet activation, overexpression of adhesion molecules, cytokines release, and leukocyte adherence. Thus, the activation of endothelial and inflammatory cells in thrombosis implicates a potential role of PARP1 activation in thrombogenesis. This review article explores the direct impact of PARP1 activation in the etiology of thrombosis and discusses PARP1-mediated endothelial dysfunction, inflammation, and epigenetic regulations in the disease manifestation. Understanding PARP1 functions associated with thrombosis may elucidate novel pathogenetic mechanisms and help in better disease management through newer therapeutic interventions targeting PARP1 activity.© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.