Pezzino Salvatore, Luca Tonia, Castorina Mariacarla, Puleo Stefano, Latteri Saverio, Castorina Sergio
Mediterranean Foundation "GB Morgagni", 95125 Catania, Italy.
Department of Medical, Surgical Sciences and Advanced Technologies "G.F. Ingrassia", University of Catania, 95123 Catania, Italy.
Life (Basel). 2024 Jan 7;14(1):93. doi: 10.3390/life14010093.
The prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) continues to rise, making it one of the most prevalent chronic liver disorders. MASLD encompasses a range of liver pathologies, from simple steatosis to metabolic dysfunction-associated steatohepatitis (MASH) with inflammation, hepatocyte damage, and fibrosis. Interestingly, the liver exhibits close intercommunication with fatty tissue. In fact, adipose tissue could contribute to the etiology and advancement of MASLD, acting as an endocrine organ that releases several hormones and cytokines, with the adipokines assuming a pivotal role. The levels of adipokines in the blood are altered in people with MASLD, and recent research has shed light on the crucial role played by adipokines in regulating energy expenditure, inflammation, and fibrosis in MASLD. However, MASLD disease is a multifaceted condition that affects various aspects of health beyond liver function, including its impact on hemostasis. The alterations in coagulation mechanisms and endothelial and platelet functions may play a role in the increased vulnerability and severity of MASLD. Therefore, more attention is being given to imbalanced adipokines as causative agents in causing disturbances in hemostasis in MASLD. Metabolic inflammation and hepatic injury are fundamental components of MASLD, and the interrelation between these biological components and the hemostasis pathway is delineated by reciprocal influences, as well as the induction of alterations. Adipokines have the potential to serve as the shared elements within this complex interrelationship. The objective of this review is to thoroughly examine the existing scientific knowledge on the impairment of hemostasis in MASLD and its connection with adipokines, with the aim of enhancing our comprehension of the disease.
代谢功能障碍相关脂肪性肝病（MASLD）的患病率持续上升，使其成为最常见的慢性肝病之一。MASLD涵盖一系列肝脏病变，从单纯性脂肪变性到伴有炎症、肝细胞损伤和纤维化的代谢功能障碍相关脂肪性肝炎（MASH）。有趣的是，肝脏与脂肪组织之间存在密切的相互作用。事实上，脂肪组织可能参与MASLD的病因和进展，作为一个释放多种激素和细胞因子的内分泌器官，其中脂肪因子起着关键作用。MASLD患者血液中的脂肪因子水平发生改变，最近的研究揭示了脂肪因子在调节MASLD的能量消耗、炎症和纤维化中所起的关键作用。然而，MASLD是一种多方面的疾病，它影响肝功能以外的健康各个方面，包括对止血的影响。凝血机制以及内皮和血小板功能的改变可能在MASLD的易感性增加和病情严重程度方面发挥作用。因此，人们越来越关注失衡的脂肪因子作为MASLD止血紊乱的致病因素。代谢炎症和肝损伤是MASLD的基本组成部分，这些生物学成分与止血途径之间的相互关系通过相互影响以及诱导改变来描述。脂肪因子有可能成为这种复杂相互关系中的共同因素。本综述的目的是全面审视关于MASLD中止血功能受损及其与脂肪因子联系的现有科学知识，以增进我们对该疾病的理解。
