ArticleCell death & disease2026
LincRNA-EPS alleviates osteoclastogenesis under inflammatory microenvironment through preventing excessive iron metabolism.
Article in Cell death & disease, 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
The precise regulation of bone homeostasis and the balance between bone resorption and formation in periodontitis remain unclear. This study explores the role of long intergenic noncoding RNA-erythroid prosurvival (lincRNA-EPS) in inflammatory osteoclastogenesis and bone resorption. LincRNA-EPS knockout (KO) worsened LPS-induced alveolar bone resorption in vivo and osteoclast differentiation in vitro. Transcriptomics and protein sequencing showed dysregulated osteoclastogenesis and iron homeostasis without lincRNA-EPS, marked by increased expression of Lcn2. Knockdown of Lcn2 in osteoclast precursors (OCPs) resulted in a reduction in the level of iron metabolism and osteoclastogenesis; however, the regulatory response was delayed in KO cells. Correspondingly, overexpression of lincRNA-EPS accelerated the regulation of iron metabolism. Further, reducing Lcn2 levels in wildtype mice alleviated periodontitis-related bone loss, but not in KO mice. Taken together, we identified the critical role of lincRNA-EPS in regulating osteoclastogenesis under inflammatory environment, by preventing excessive iron metabolism caused by Lcn2.
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