Fibrosis is the final pathological outcome and major cause of morbidity and mortality in many common and chronic inflammatory, immune-mediated, and metabolic diseases. Despite the growing incidence of fibrotic diseases and extensive research efforts, there remains a lack of effective therapies that improve survival. The application of omics technologies has revolutionized our approach to identifying previously unknown therapeutic targets and potential disease biomarkers. The application of metabolomics, in particular, has improved our understanding of disease pathomechanisms and garnered a wave of scientific interest in the role of metabolism in the biology of myofibroblasts, the key effector cells of the fibrogenic response. Emerging evidence suggests that alterations in metabolism not only are a feature of but also may play an influential role in the pathogenesis of fibrosis, most notably in idiopathic pulmonary fibrosis (IPF), the most rapidly progressive and fatal of all fibrotic conditions. This review will detail the role of key metabolic pathways, their alterations in myofibroblasts, and the potential this new knowledge offers for the development of antifibrotic therapeutic strategies.

纤维化是许多常见和慢性炎症、免疫介导和代谢疾病的最终病理结果和发病率和死亡率的主要原因。尽管纤维化疾病的发病率越来越高，研究工作也越来越广泛，但仍然缺乏提高生存率的有效疗法。组学技术的应用彻底改变了我们识别以前未知的治疗靶点和潜在疾病生物标志物的方法。尤其是代谢组学的应用，提高了我们对疾病发病机制的理解，并引起了对代谢在肌成纤维细胞生物学中的作用的科学兴趣，肌成纤维细胞是纤维化反应的关键效应细胞。新出现的证据表明，新陈代谢的改变不仅是纤维化的一个特征，而且可能在纤维化的发病机制中发挥重要作用，尤其是在特发性肺纤维化 (IPF) 中，这是所有纤维化病症中进展最快和致命的。本综述将详细介绍关键代谢途径的作用、它们在肌成纤维细胞中的变化，以及这一新知识为开发抗纤维化治疗策略提供的潜力。