ArticleCell biology and toxicology2026
LncRNA-Gm5532 deficiency alleviates bone resorption by inhibiting mitochondrial respiration through iASPP/NRF2.
Article in Cell biology and toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed.
- The recent progression of extracellular vesicles application in osteoporosis.Frontiers in pharmacology · 2026Review
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7 authors.
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Abstract
Osteoporosis, characterized by excessive osteoclast activity and bone resorption, is closely linked to mitochondrial respiration. The long non-coding RNA Gm5532 (Gm5532) has been implicated in osteoclast differentiation, but its role in mitochondrial function remains unclear. This study aimed to elucidate the mechanism by which Gm5532 regulates bone resorption through iron metabolism and mitochondrial respiration, focusing on its interaction with iASPP and the NRF2 signaling pathway. Here, we show that Gm5532 KO alleviates bone loss in aged, ovariectomized, and iron-overloaded mice by reducing osteoclast formation and activity. Mechanistically, Gm5532 directly interacts with the RNA-binding protein iASPP. This interaction modulates the KEAP1/NRF2 axis, leading to the destabilization of NRF2. Gm5532 KO enhances iASPP-KEAP1 binding, thereby stabilizing NRF2 and upregulating its target genes: Ftl, Fth, and Fpn1. This cascade reduces the intracellular labile iron pool. Iron deficiency suppresses mitochondrial biogenesis and respiration, and ultimately, inhibites osteoclast differentiation. In summary, Gm5532 functions as a critical regulator of bone resorption through its modulation of iron homeostasis and mitochondrial respiration. Our study uncovers a novel Gm5532-iASPP-NRF2 signaling axis that links iron metabolism to mitochondrial respiration and osteoclast function, offering a promising potential therapeutic target for osteoporosis.
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