肺纤维化和糖尿病:两枚面孔相同的硬币

Archives of internal medicine research Pub Date : 2024-01-01 Epub Date: 2024-03-16 DOI:10.26502/aimr.0165
Yssel Mendoza Mari, Marcel P Fraix, Devendra K Agrawal
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引用次数: 0

摘要

特发性肺纤维化(IPF)是一种长期疾病,其复杂的病理生理学由多种分子因素组成,导致细胞外基质沉积、肺功能丧失并最终导致患者死亡。尽管吡非尼酮(pirfenidone)和宁替达尼(nintedanib)已被批准用于治疗这种疾病,但肺移植是完全恢复呼吸能力和提高生活质量的唯一长期解决方案。患上 IPF 的风险因素之一是原有的糖尿病。IPF 和糖尿病具有相似的病理损伤机制,包括炎症、内质网应激、线粒体功能衰竭、氧化应激、衰老以及糖化蛋白通过受体发出的信号。在这篇重要的综述文章中,我们提供了有关这种相互关系的信息,研究了在这两种疾病中发挥重要作用的分子介质,并确定了开发潜在药物的目标。我们回顾了研究 IPF 进展的临床试验结果,以及如何利用新型分子阻止这一过程。研究结果强调了早期检测和同时针对多个治疗靶点的重要性,以获得更好的疗效并有可能逆转肺纤维化。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Pulmonary Fibrosis and Diabetes Mellitus: Two coins with the same face.

Idiopathic pulmonary fibrosis (IPF) constitutes a long-term disease with a complex pathophysiology composed of multiple molecular actors that lead to the deposition of extracellular matrix, the loss of pulmonary function and ultimately the patient's death. Despite the approval of pirfenidone and nintedanib for the treatment of the disease, lung transplant is the only long-term solution to fully recover the respiratory capacity and gain quality of life. One of the risk factors for the development of IPF is the pre-existing condition of diabetes mellitus. Both, IPF and diabetes mellitus, share similar pathological damage mechanisms, including inflammation, endoplasmic reticulum stress, mitochondrial failure, oxidative stress, senescence and signaling from glycated proteins through receptors. In this critical review article, we provide information about this interrelationship, examining molecular mediators that play an essential role in both diseases and identify targets of interest for the development of potential drugs. We review the findings of clinical trials examining the progression of IPF and how novel molecules may be used to stop this process. The results highlight the importance of early detection and addressing multiple therapeutic targets simultaneously to achieve better therapeutic efficacy and potentially reverse lung fibrosis.

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