{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n Long noncoding RNAs (lncRNAs) can exert regulatory functions in complex diseases through a variety of mechanisms, including cis‐regulation of adjacent protein‐coding genes and participation in competing endogenous RNA (ceRNA) networks. In one study, a lncRNA adjacent to a key protein‐coding gene that activates growth factor and mTOR‐dependent signaling was shown to be upregulated in patients with idiopathic pulmonary fibrosis (IPF), suggesting that such lncRNAs contribute to aging‐associated fibrotic processes by modulating the expression of nearby genes (1). In a separate investigation focused on ischemic cardiomyopathy (ICM), a strategy integrating RNA‐Seq and miRNA‐Seq data identified several susceptibility biomarkers, including lncRNAs that are tightly correlated with candidate ICM genes, thereby highlighting their function within ceRNA triplets that impact the disease’s gene regulatory networks (2). By extrapolation, ADAMTSL4‑AS1—a lncRNA that, like other regulatory RNAs in these studies, may modulate its adjacent coding gene and participate in ceRNA interactions—could play a dual role in disease biology. On one hand, it might influence aging‐related processes and fibrotic remodeling in pulmonary tissue by directly regulating neighboring genes. On the other hand, its involvement in ceRNA networks may render it a valuable biomarker for the susceptibility to and early diagnosis of ICM. Together, these findings underscore the importance of lncRNAs such as ADAMTSL4‑AS1 as multifunctional regulators that not only affect disease progression through local gene modulation but also by orchestrating complex post‐transcriptional networks in diverse pathological contexts (1,2).\n "}, {"type": "rg", "children": []}]}]}