Metabolic dysfunction−associated liver disease and diabetes: Matrix remodeling, fibrosis, and therapeutic implications,Annals of the New York Academy of Sciences

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Metabolic dysfunction−associated liver disease and diabetes: Matrix remodeling, fibrosis, and therapeutic implications
Annals of the New York Academy of Sciences ( IF 4.1 ) Pub Date : 2024-07-12 , DOI: 10.1111/nyas.15184
Weiguo Fan _{1,

2} , Toby M Bradford ₁ , Natalie J Török _{1,

2}

Affiliation

Metabolic dysfunction−associated liver disease (MASLD) and steatohepatitis (MASH) are becoming the most common causes of chronic liver disease in the United States and worldwide due to the obesity and diabetes epidemics. It is estimated that by 2030 close to 100 million people might be affected and patients with type 2 diabetes are especially at high risk. Twenty to 30% of patients with MASLD can progress to MASH, which is characterized by steatosis, necroinflammation, hepatocyte ballooning, and in advanced cases, fibrosis progressing to cirrhosis. Clinically, it is recognized that disease progression in diabetic patients is accelerated and the role of various genetic and epigenetic factors, as well as cell–matrix interactions in fibrosis and stromal remodeling, have recently been recognized. While there has been great progress in drug development and clinical trials for MASLD/MASH, the complexity of these pathways highlights the need to improve diagnosis/early detection and develop more successful antifibrotic therapies that not only prevent but reverse fibrosis.

中文翻译：

代谢功能障碍相关的肝病和糖尿病：基质重塑、纤维化和治疗意义

由于肥胖和糖尿病的流行，代谢功能障碍相关肝病（MASLD）和脂肪性肝炎（MASH）正在成为美国和世界范围内慢性肝病的最常见原因。据估计，到 2030 年，将有近 1 亿人可能受到影响，其中 2 型糖尿病患者的风险尤其高。 20% 至 30% 的 MASLD 患者可进展为 MASH，其特点是脂肪变性、坏死性炎症、肝细胞膨胀，在晚期病例中，纤维化进展为肝硬化。临床上，人们认识到糖尿病患者的疾病进展会加速，并且最近认识到各种遗传和表观遗传因素以及细胞-基质相互作用在纤维化和基质重塑中的作用。尽管 MASLD/MASH 的药物开发和临床试验取得了巨大进展，但这些途径的复杂性突出表明需要改进诊断/早期检测并开发更成功的抗纤维化疗法，不仅可以预防纤维化，还可以逆转纤维化。

更新日期：2024-07-12

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