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<p><i>LOXL2Δ13</i>, a splice variant of Lysyl-oxidase like-2 (<i>LOXL2</i>), enhances glucose metabolism and induces adipose depletion in mice. The precise role of <i>LOXL2Δ13</i> in lipid metabolism is unclear. Through multi-omics integration, we analyzed the transcriptome, metabolome, proteome, and protein modifications profiles in <i>LOXL2Δ13</i> overexpression mice. Molecular dynamics simulation and interaction mass spectrometry confirmed key biomarkers influenced by <i>LOXL2Δ13</i>. Here, <i>LOXL2Δ13</i> was found to cause diglyceride and glycerophospholipid accumulation and alter kinase activities in pathways. Differentially expressed genes, proteins, and metabolites were enriched in lipid metabolism pathways, indicating <i>LOXL2Δ13</i> influences metabolic enzyme activity by regulating protein expression and modifications. Further immunoprecipitation assay demonstrated that four proteins (Itpr1, Acat1, Canx, and Pdia3) directly interact with <i>LOXL2∆13</i>. This suggests that <i>LOXL2∆13</i> can regulate lipid metabolic pathways through direct interactions affecting the activity of these key proteins, which in turn induce alterations in their phosphorylation or acetylation modifications, thereby affecting the lipid metabolic pathways.</p><p></p>

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Integrating multi-omics to reveal the molecular mechanism of lipid metabolism regulated by a splice variant of Lysyl-oxidase like-2, LOXL2Δ13

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月21日

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  • Yang Chen,
  • Liu Peng,
  • Jian-Zhong He,
  • Xiao-Dong Wu,
  • Xing Xu,
  • Geng Dong,
  • En-Min Li,
  • Li-Yan Xu

摘要

LOXL2Δ13, a splice variant of Lysyl-oxidase like-2 (LOXL2), enhances glucose metabolism and induces adipose depletion in mice. The precise role of LOXL2Δ13 in lipid metabolism is unclear. Through multi-omics integration, we analyzed the transcriptome, metabolome, proteome, and protein modifications profiles in LOXL2Δ13 overexpression mice. Molecular dynamics simulation and interaction mass spectrometry confirmed key biomarkers influenced by LOXL2Δ13. Here, LOXL2Δ13 was found to cause diglyceride and glycerophospholipid accumulation and alter kinase activities in pathways. Differentially expressed genes, proteins, and metabolites were enriched in lipid metabolism pathways, indicating LOXL2Δ13 influences metabolic enzyme activity by regulating protein expression and modifications. Further immunoprecipitation assay demonstrated that four proteins (Itpr1, Acat1, Canx, and Pdia3) directly interact with LOXL2∆13. This suggests that LOXL2∆13 can regulate lipid metabolic pathways through direct interactions affecting the activity of these key proteins, which in turn induce alterations in their phosphorylation or acetylation modifications, thereby affecting the lipid metabolic pathways.