MicroRNAs in IPF and Lung Cancer: Convergent and Divergent Mechanisms: a systematic review.
TL;DR
A framework for understanding miRNA dysregulation in IPF and LC is provided, with direct implications for biomarker validation and therapeutic targeting, by systematically integrating mechanistic and regulatory evidence.
Abstract
Idiopathic pulmonary fibrosis (IPF) and lung cancer (LC) are distinct pathological entities; however, growing evidence indicates that they share convergent cellular and molecular mechanisms. As central post-transcriptional regulators microRNAs (miRNAs) orchestrate critical pathogenetic processes including epithelial-mesenchymal transition (EMT), TGF-β signaling, fibroblast activation, and extracellular matrix remodeling. Circulating miRNA signatures represents a promising class of minimally invasive biomarkers for early detection, risk stratification, and disease monitoring, while emerging therapeutic strategies based on miRNA mimics or inhibitors have shown encouraging results in preclinical models. Understanding the complex interplay of miRNAs at the interface between fibrogenesis and oncogenesis may facilitate the development of novel translational approaches, ultimately improving patient outcomes in both IPF and LC. Dysregulation of specific miRNAs has been implicated in both IPF and LC, some of which with concordant expression patterns, such as miR-21,miR-155, and miR-200 promoting fibrosis and tumor progression, and others exhibiting divergent roles, including miR-204 5-p and members of the miR-20a e miR-425, exerting opposing effects in fibrotic and neoplastic contexts. By systematically integrating mechanistic and regulatory evidence, this review provides a framework for understanding miRNA dysregulation in IPF and LC, with direct implications for biomarker validation and therapeutic targeting.