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Nucleoid-phagy: a novel safeguard against mitochondrial DNA-Induced inflammation.
Liu, Hao; Xie, Jianming; Zhen, Cien; Zeng, Lin; Fan, Hualin; Zhuang, Haixia; Feng, Du.
Afiliación
  • Liu H; Translational Medicine Center, Huaihe Hospital of Henan University, Henan University, Kaifeng, China.
  • Xie J; State Key Laboratory of Respiratory Disease, Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China.
  • Zhen C; Department of Anesthesiology, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
  • Zeng L; Qingyuan People's Hospital, The Sixth Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
  • Fan H; State Key Laboratory of Respiratory Disease, Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China.
  • Zhuang H; The Affiliated Traditional Chinese Medicine Hospital, Guangzhou Medical University, Guangzhou, China.
  • Feng D; State Key Laboratory of Respiratory Disease, Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China.
Autophagy ; : 1-3, 2024 Sep 03.
Article en En | MEDLINE | ID: mdl-39225184
ABSTRACT
Mitochondria, the powerhouses of the cell, play pivotal roles in cellular processes ranging from energy production to innate immunity. Their unique double-membrane structure typically sequesters mitochondrial DNA (mtDNA) from the rest of the cell. However, under oxidative or immune stress, mtDNA can escape into the cytoplasm, posing a threat as a potential danger signal. The accumulation of cytoplasmic mtDNA can disrupt cellular immune balance and trigger cell death. Our research unveils a novel quality control mechanism, which we term "nucleoid-phagy", that safeguards cellular homeostasis by clearing mislocalized mtDNA. We demonstrate that TFAM, a key protein involved in mtDNA folding and wrapping, accompanies mtDNA into the cytoplasm under stress conditions. Remarkably, TFAM acts as an autophagy receptor, interacting with LC3B to facilitate the autophagic clearance of cytoplasmic mtDNA, thereby preventing the activation of the pro-inflammatory CGAS-STING1 pathway. This study provides unprecedented insights into cytoplasmic mtDNA quality control and offers new perspectives on mitigating inflammatory responses in mitochondrial-related diseases.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Autophagy Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Autophagy Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos