ArticleNature communications2025
PNPLA7 mediates Parkin-mitochondrial recruitment in adipose tissue for mitophagy and inhibits browning.
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Article in Nature communications, 2025. 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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- Mitochondria-associated endoplasmic reticulum membrane (MAM): roles in innate immunity dysregulation.Cell communication and signaling : CCS · 2026Review
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27 authors.
Xuetao Ji *The Key Laboratory of Rare Metabolic Disease, Department of Molecular Biology and Biochemistry, Jiangsu Key Laboratory of Molecular Targets and Intervention for Metabolic Diseases, The Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, Jiangsu, 211166, China.
Xu Zhang *The Key Laboratory of Rare Metabolic Disease, Department of Molecular Biology and Biochemistry, Jiangsu Key Laboratory of Molecular Targets and Intervention for Metabolic Diseases, The Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, Jiangsu, 211166, China.
Tong ZhangThe Key Laboratory of Rare Metabolic Disease, Department of Molecular Biology and Biochemistry, Jiangsu Key Laboratory of Molecular Targets and Intervention for Metabolic Diseases, The Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, Jiangsu, 211166, China.
Yao XueThe Key Laboratory of Rare Metabolic Disease, Department of Molecular Biology and Biochemistry, Jiangsu Key Laboratory of Molecular Targets and Intervention for Metabolic Diseases, The Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, Jiangsu, 211166, China.
Mengping HeThe Key Laboratory of Rare Metabolic Disease, Department of Molecular Biology and Biochemistry, Jiangsu Key Laboratory of Molecular Targets and Intervention for Metabolic Diseases, The Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, Jiangsu, 211166, China.
Chaopu LiThe Key Laboratory of Rare Metabolic Disease, Department of Molecular Biology and Biochemistry, Jiangsu Key Laboratory of Molecular Targets and Intervention for Metabolic Diseases, The Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, Jiangsu, 211166, China.
Yun HuangThe Key Laboratory of Rare Metabolic Disease, Department of Molecular Biology and Biochemistry, Jiangsu Key Laboratory of Molecular Targets and Intervention for Metabolic Diseases, The Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, Jiangsu, 211166, China.
Haoyu WangThe Key Laboratory of Rare Metabolic Disease, Department of Molecular Biology and Biochemistry, Jiangsu Key Laboratory of Molecular Targets and Intervention for Metabolic Diseases, The Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, Jiangsu, 211166, China.
Jing JuThe Key Laboratory of Rare Metabolic Disease, Department of Molecular Biology and Biochemistry, Jiangsu Key Laboratory of Molecular Targets and Intervention for Metabolic Diseases, The Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, Jiangsu, 211166, China.
Li'e CaiThe Key Laboratory of Rare Metabolic Disease, Department of Molecular Biology and Biochemistry, Jiangsu Key Laboratory of Molecular Targets and Intervention for Metabolic Diseases, The Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, Jiangsu, 211166, China.
Yuzhu WangThe Key Laboratory of Rare Metabolic Disease, Department of Molecular Biology and Biochemistry, Jiangsu Key Laboratory of Molecular Targets and Intervention for Metabolic Diseases, The Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, Jiangsu, 211166, China.
Ning WangThe Key Laboratory of Rare Metabolic Disease, Department of Molecular Biology and Biochemistry, Jiangsu Key Laboratory of Molecular Targets and Intervention for Metabolic Diseases, The Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, Jiangsu, 211166, China.
Lijuan FanThe Key Laboratory of Rare Metabolic Disease, Department of Molecular Biology and Biochemistry, Jiangsu Key Laboratory of Molecular Targets and Intervention for Metabolic Diseases, The Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, Jiangsu, 211166, China.
Hui TongThe Key Laboratory of Rare Metabolic Disease, Department of Molecular Biology and Biochemistry, Jiangsu Key Laboratory of Molecular Targets and Intervention for Metabolic Diseases, The Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, Jiangsu, 211166, China.
Heng FanInstitute of Human Stem Cells, General Hospital of Ningxia Medical University, Yinchuan, Ningxia, China.
Qinsheng ChenState Key Laboratory of Genetic Engineering, School of Life Sciences, Human Phenome Institute, Zhangjiang Fudan International Innovation Center, metabolomics and Systems Biology Laboratory at Shanghai International Centre for Molecular Phenomics, Zhongshan Hospital, Fudan University, Shanghai, China.
Qinwei LuState Key Laboratory of Genetic Engineering, School of Life Sciences, Human Phenome Institute, Zhangjiang Fudan International Innovation Center, metabolomics and Systems Biology Laboratory at Shanghai International Centre for Molecular Phenomics, Zhongshan Hospital, Fudan University, Shanghai, China.
Cong LiState Key Laboratory of Genetic Engineering, School of Life Sciences, Human Phenome Institute, Zhangjiang Fudan International Innovation Center, metabolomics and Systems Biology Laboratory at Shanghai International Centre for Molecular Phenomics, Zhongshan Hospital, Fudan University, Shanghai, China.
Huiru TangState Key Laboratory of Genetic Engineering, School of Life Sciences, Human Phenome Institute, Zhangjiang Fudan International Innovation Center, metabolomics and Systems Biology Laboratory at Shanghai International Centre for Molecular Phenomics, Zhongshan Hospital, Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0002-7139-2756
Yongsheng ChangDepartment of Physiology and Pathophysiology, Tianjin Medical University, Tianjin, China.ORCID http://orcid.org/0000-0002-7846-8127
Xingxing KongState Key Laboratory of Genetic Engineering, Shanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, School of Life Sciences, Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0002-8395-0268
Hanming ShenFaculty of Health Sciences, University of Macau, Macau, China.ORCID http://orcid.org/0000-0001-7369-5227
Aihua GuThe Key Laboratory of Rare Metabolic Disease, Department of Molecular Biology and Biochemistry, Jiangsu Key Laboratory of Molecular Targets and Intervention for Metabolic Diseases, The Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, Jiangsu, 211166, China.ORCID http://orcid.org/0000-0001-7576-9998
Hui LiangDepartment of General Surgery, The First affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China.
Hongwen ZhouThe Key Laboratory of Rare Metabolic Disease, Department of Molecular Biology and Biochemistry, Jiangsu Key Laboratory of Molecular Targets and Intervention for Metabolic Diseases, The Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, Jiangsu, 211166, China.
Qian WangThe Key Laboratory of Rare Metabolic Disease, Department of Molecular Biology and Biochemistry, Jiangsu Key Laboratory of Molecular Targets and Intervention for Metabolic Diseases, The Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, Jiangsu, 211166, China. wqian@njmu.edu.cn.
John Zhong LiThe Key Laboratory of Rare Metabolic Disease, Department of Molecular Biology and Biochemistry, Jiangsu Key Laboratory of Molecular Targets and Intervention for Metabolic Diseases, The Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, Jiangsu, 211166, China. lizhong@njmu.edu.cn.ORCID http://orcid.org/0000-0003-4991-9563
Funding
No grant is acknowledged in the PubMed record.
Abstract
PINK1/Parkin-mediated ubiquitin-dependent mitophagy is a critical negative regulatory machinery for browning in the inguinal white adipose tissue (iWAT). However, the precise regulatory mechanism underlying PINK1/Parkin-mediated mitophagy during browning of iWAT remains largely unknown. Here we report that PNPLA7, an Endoplasmic Reticulum and mitochondria-associated membrane (MAM) protein, inhibits browning of iWAT by promoting PINK1/Parkin-mediated mitophagy upon cold challenge or β3-adrenergic receptor agonist treatment. With genetic manipulation in mice, we show that adipose tissue overexpressing PNPLA7 induces mitophagy, abolishes iWAT browning and interrupts adaptive thermogenesis. Conversely, conditional ablation of PNPLA7 in adipose tissue promotes browning of iWAT, resulting in enhanced adaptive thermogenesis. Mechanistically, PNPLA7 interacts with Parkin to promote mitochondrial recruitment of Parkin for mitophagy activation and mitochondria degradation by disrupting PKA-induced phosphorylation of Parkin under cold challenge. Taken together, our findings suggest that PNPLA7 is a critical regulator of mitophagy that resists cold-induced browning of iWAT, thus providing a direct mechanistic link between mitophagy and browning of iWAT.
Indexed as
Adipose Tissue, BrownAdipose Tissue, WhiteLipaseMembrane ProteinsMitochondriaMitophagyUbiquitin-Protein LigasesAnimalsCold TemperatureHumansMaleMiceMice, Inbred C57BLMice, KnockoutPhosphorylationProtein KinasesLipaseMembrane Proteinsparkin proteinProtein KinasesPTEN-Induced Putative KinaseUbiquitin-Protein Ligases
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