代谢功能障碍相关脂肪性肝炎 (MASH) 是一种严重的肝病，由于其有可能进展为晚期纤维化，导致肝硬化和肝癌，因此对全球健康构成威胁。单细胞方法学、精细疾病模型以及遗传和表观遗传见解的最新进展提供了对 MASH 纤维发生的细致了解，MASH 肝脏中显着的细胞异质性提供了潜在的可靶向细胞间相互作用和行为。与纤维发生不同，尽管最近已经确定了抗纤维化靶标，但 MASH 中纤维化消退的潜在机制仍知之甚少。完善的抗纤维化治疗框架可以实现无创评估和靶向治疗，从而保护肝细胞功能并恢复肝脏结构的完整性。

Metabolic dysfunction-associated steatohepatitis (MASH) is a severe form of liver disease that poses a global health threat because of its potential to progress to advanced fibrosis, leading to cirrhosis and liver cancer. Recent advances in single-cell methodologies, refined disease models, and genetic and epigenetic insights have provided a nuanced understanding of MASH fibrogenesis, with substantial cellular heterogeneity in MASH livers providing potentially targetable cell-cell interactions and behavior. Unlike fibrogenesis, mechanisms underlying fibrosis regression in MASH are still inadequately understood, although antifibrotic targets have been recently identified. A refined antifibrotic treatment framework could lead to noninvasive assessment and targeted therapies that preserve hepatocellular function and restore the liver's architectural integrity.