Research Service, Harry S. Truman Memorial Veterans' Hospital, Columbia, MO, United States.
Comparative Medicine Program, Department of Veterinary Pathobiology, University of Missouri, Columbia, MO, United States.
Front Endocrinol (Lausanne). 2021 Oct 20;12:770740. doi: 10.3389/fendo.2021.770740. eCollection 2021.
Non-alcoholic fatty liver disease (NAFLD) is a multimorbidity disorder ranging from excess accumulation of fat in the liver (steatosis) to steatohepatitis (NASH) and end-stage cirrhosis, and the development of hepatocellular carcinoma (HCC) in a subset of patients. The defining features of NASH are inflammation and progressive fibrosis. Currently, no pharmaceutical therapies are available for NAFLD, NASH and HCC; therefore, developing novel treatment strategies is desperately needed. Reversion Inducing Cysteine Rich Protein with Kazal motifs (RECK) is a well-known modifier of the extracellular matrix in hepatic remodeling and transition to HCC. More recently, its role in regulating inflammatory and fibrogenic processes has emerged. Here, we summarize the most relevant findings that extend our current understanding of RECK as a regulator of inflammation and fibrosis, and its induction as a potential strategy to blunt the development and progression of NASH and HCC.
非酒精性脂肪性肝病（NAFLD）是一种多系统疾病，其范围从肝脏脂肪过度堆积（脂肪变性）到脂肪性肝炎（NASH）和终末期肝硬化，以及一部分患者发生肝细胞癌（HCC）。NASH 的特征性表现为炎症和进行性纤维化。目前，尚无针对 NAFLD、NASH 和 HCC 的药物治疗方法；因此，迫切需要开发新的治疗策略。富含半胱氨酸的 Kazal 基序的诱导回复蛋白（RECK）是肝重塑和向 HCC 转化过程中细胞外基质的重要调节因子。最近，其在调节炎症和纤维生成过程中的作用也逐渐显现。本文总结了 RECK 作为炎症和纤维化调节剂的最相关研究结果，以及将其诱导作为一种潜在策略来抑制 NASH 和 HCC 发展和进展的研究进展。
