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Background <p>Periodontitis is a chronic inflammatory disease characterized by oxidative stress, immune dysregulation, and progressive alveolar bone loss. Conventional treatments such as mechanical debridement and antimicrobial therapy often fail to reverse bone destruction or restore periodontal homeostasis, underscoring the need for novel therapeutic strategies. Mitochondria have emerged as critical regulators of immune–metabolic signaling, and their genetic modification offers new opportunities for targeted intervention.</p> Results <p>This study explored mitochondria engineered to overexpress aquaporin 1 (ovAQP1-mito) as a therapeutic approach for periodontitis. In vitro, ovAQP1-mito modulated macrophage activity and inhibited receptor activator of nuclear factor κB ligand (RANKL)-induced osteoclast differentiation, suggesting direct immunometabolic effects. In vivo, transplantation of ovAQP1-mito into a ligature-induced mouse model attenuated alveolar bone loss, reduced inflammatory cell infiltration, and preserved periodontal architecture. Mechanistic studies further demonstrated that ovAQP1-mito enhanced SigmaR1 expression, facilitated endoplasmic reticulum–mitochondria communication, and suppressed osteoclastogenic signaling.</p> Conclusion <p>These findings indicate that ovAQP1-mito exerts dual regulatory effects by mitigating inflammation and bone resorption through ER-mito contacts and immune–metabolic modulation. Such mitochondria-based engineering may represent a promising therapeutic strategy for periodontitis and potentially other inflammatory bone disorders.</p> Graphical abstract <p></p>

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Transplantation of AQP1-overexpressing mitochondria attenuates periodontitis-associated bone loss by regulating mitochondria-ER contacts of macrophages

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月28日

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  • Shuqing Yang,
  • Ming Zhang,
  • Junbin Wei,
  • Le Yu,
  • Houze Li,
  • Shuxuan Rong,
  • Lingling Chen,
  • Tingting Zhao,
  • Junkun Zhan,
  • Xiaoxiao Wang,
  • Yunyi Xie,
  • Yan Wang

摘要

Background

Periodontitis is a chronic inflammatory disease characterized by oxidative stress, immune dysregulation, and progressive alveolar bone loss. Conventional treatments such as mechanical debridement and antimicrobial therapy often fail to reverse bone destruction or restore periodontal homeostasis, underscoring the need for novel therapeutic strategies. Mitochondria have emerged as critical regulators of immune–metabolic signaling, and their genetic modification offers new opportunities for targeted intervention.

Results

This study explored mitochondria engineered to overexpress aquaporin 1 (ovAQP1-mito) as a therapeutic approach for periodontitis. In vitro, ovAQP1-mito modulated macrophage activity and inhibited receptor activator of nuclear factor κB ligand (RANKL)-induced osteoclast differentiation, suggesting direct immunometabolic effects. In vivo, transplantation of ovAQP1-mito into a ligature-induced mouse model attenuated alveolar bone loss, reduced inflammatory cell infiltration, and preserved periodontal architecture. Mechanistic studies further demonstrated that ovAQP1-mito enhanced SigmaR1 expression, facilitated endoplasmic reticulum–mitochondria communication, and suppressed osteoclastogenic signaling.

Conclusion

These findings indicate that ovAQP1-mito exerts dual regulatory effects by mitigating inflammation and bone resorption through ER-mito contacts and immune–metabolic modulation. Such mitochondria-based engineering may represent a promising therapeutic strategy for periodontitis and potentially other inflammatory bone disorders.

Graphical abstract