ArticleMolecular biology reports2026
lncRNA HOTAIR promotes airway remodeling by regulating metabolic reprogramming through the FUS/HK2 axis in airway smooth muscle cells.
Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundAirway remodeling is a critical pathological feature of chronic airway diseases and is closely associated with irreversible airflow limitation. Increasing evidence indicates that metabolic reprogramming contributes to airway smooth muscle cell (ASMC) remodeling; however, the underlying regulatory mechanisms remain incompletely understood.
methodsHuman ASMCs were stimulated with platelet-derived growth factor-BB (PDGF-BB) to establish an in vitro remodeling model. HOTAIR expression was manipulated using siRNA-mediated knockdown, while FUS and HK2 were restored by plasmid overexpression. Cell viability, proliferation, migration, glycolytic metabolism, and remodeling-associated protein expression were assessed using CCK-8, EdU staining, Transwell assays, Seahorse extracellular flux analysis, qRT-PCR, and western blotting. RNA immunoprecipitation (RIP) and mRNA stability assays were performed to investigate the interaction among HOTAIR, FUS, and HK2.
resultsHOTAIR expression was significantly upregulated in PDGF-BB-stimulated ASMCs. HOTAIR knockdown markedly inhibited ASMC proliferation, migration, and ECM remodeling, with reduced expression of Collagen I, Fibronectin, MMP9, and α-SMA. HOTAIR silencing suppressed glucose uptake, lactate production, ATP generation, and ECAR while partially restoring mitochondrial oxidative phosphorylation. FUS directly bound both HOTAIR and HK2 mRNA; HOTAIR depletion accelerated HK2 mRNA degradation, whereas FUS restoration rescued HK2 mRNA stability. Re-expression of either FUS or HK2 reversed the inhibitory effects of HOTAIR silencing on glycolytic metabolism and ASMC remodeling phenotypes.
conclusionHOTAIR promotes PDGF-BB-induced glycolytic reprogramming and airway smooth muscle remodeling by stabilizing HK2 mRNA through the RNA-binding protein FUS. T These findings suggest that the HOTAIR/FUS/HK2 axis contributes to PDGF-BB-induced ASMC remodeling and may represent a potential therapeutic target.
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