Gill Sumeen Kaur, Gomer Richard H
Department of Biology, Texas A&M University, College Station, TX, USA.
Department of Biology, Texas A&M University, College Station, TX, USA.
Trends Mol Med. 2025 Jul;31(7):640-651. doi: 10.1016/j.molmed.2024.11.012. Epub 2024 Dec 16.
Idiopathic pulmonary fibrosis (IPF) is a progressive and debilitating lung disease characterized by excessive extracellular matrix deposition and tissue scarring. The median survival of patients with IPF is only 4.5 years following diagnosis, and effective treatment options are scarce. Recent studies found aberrant translation of specific mRNAs in various fibrosing diseases, highlighting the role of key translational regulators, including RNA binding proteins (RBPs), microRNAs, long noncoding RNAs, and transcript modifications. Notably, when inhibited, 10 profibrotic RBPs cause a significant attenuation of fibrosis, illuminating potential therapeutic targets. In this review, we describe translational regulation in fibrosis and highlight a model where a conserved evolutionary mechanism may explain this regulation.
特发性肺纤维化（IPF）是一种进行性且使人衰弱的肺部疾病，其特征为细胞外基质过度沉积和组织瘢痕形成。IPF患者确诊后的中位生存期仅为4.5年，且有效的治疗选择匮乏。最近的研究发现，特定mRNA在各种纤维化疾病中存在异常翻译，这凸显了关键翻译调节因子的作用，包括RNA结合蛋白（RBP）、微小RNA、长链非编码RNA和转录修饰。值得注意的是，当受到抑制时，10种促纤维化RBP会使纤维化显著减轻，这为潜在的治疗靶点提供了线索。在本综述中，我们描述了纤维化中的翻译调控，并强调了一种保守的进化机制可能解释这种调控的模型。
