ArticleJournal of bioenergetics and biomembranes2026
DNA methylation-mediated silencing of MALAT1 promotes dexamethasone-induced growth plate chondrocyte ferroptosis via miR-124-3p/LPCAT3.
Article in Journal of bioenergetics and biomembranes, 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
Dexamethasone (Dex) causes growth plate injury and growth retardation in children, yet the underlying epigenetic and post-transcriptional mechanisms remain poorly defined. This study addresses this gap by dissecting the MALAT1/miR-124-3p/LPCAT3 axis in Dex-induced chondrocyte ferroptosis. Primary rat growth plate chondrocytes and 2-week-old male Sprague-Dawley rats were treated with Dex. DNA methylation of the MALAT1 promoter was assessed by MSP analysis. Gain- and loss-of-function studies, CCK-8, ferroptosis markers and luciferase reporter assays were performed in vitro. In vivo, tibial growth plate morphology, zone-specific heights, systemic growth parameters and LPCAT3 expression were evaluated. The results showed that Dex reduced chondrocyte viability and suppressed MALAT1 expression in a dose-dependent manner, accompanied by hypermethylation of one CpG islands in the MALAT1 promoter. Treatment with 5-Aza-2'-deoxycytidine (5-Aza) restored MALAT1 expression and reduced methylation levels. MALAT1 overexpression attenuated Dex-induced ferroptosis, as evidenced by decreased Fe²⁺ and MDA levels and restored SLC7A11 and Gpx4 expression. Mechanistically, MALAT1 directly binds to miR-124-3p, which targets LPCAT3. miR-124-3p mimics abolished the protective effects of MALAT1, while LPCAT3 overexpression reversed the inhibitory effects of miR-124-3p mimics on cell viability and ferroptosis markers. In vivo, Dex reduced growth plate thickness, tibial length, and body weight gain, while both MALAT1 overexpression and 5-Aza treatment attenuated these deficits and restored LPCAT3 expression. In conclusion, DNA methylation-mediated MALAT1 downregulation promotes Dex-induced chondrocyte ferroptosis via the miR-124-3p/LPCAT3 axis. Targeting this pathway may represent a preclinically promising therapeutic strategy that warrants further investigation in glucocorticoid-induced growth retardation in children.
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