Equipe Labellisée par la Ligue Contre le Cancer, Université de Paris, Sorbonne Université, Inserm U1138, Centre de Recherche des Cordeliers, Paris, France; Metabolomics and Cell Biology Platforms, Institut Gustave Roussy, Villejuif, France; Pôle de Biologie, Hôpital Européen Georges Pompidou, AP-HP, Paris, France; Suzhou Institute for Systems Medicine, Chinese Academy of Medical Sciences, Suzhou, China; Karolinska Institute, Department of Women's and Children's Health, Karolinska University Hospital, Stockholm, Sweden.
Suzhou Institute for Systems Medicine, Chinese Academy of Medical Sciences, Suzhou, China; Faculty of Medicine, Université Paris Saclay, Le Kremlin-Bicêtre, France; Gustave Roussy Comprehensive Cancer Institute, Villejuif, France; INSERM U1015, Villejuif, France; Center of Clinical Investigations in Biotherapies of Cancer (CICBT) 1428, Villejuif, France.
Cell Metab. 2020 Jul 7;32(1):4-5. doi: 10.1016/j.cmet.2020.04.016. Epub 2020 May 12.
Bharath et al., 2020 report that CD4 T lymphocytes from aged individuals exhibit defective mitochondrial autophagy, resulting in altered redox metabolism and upregulation of TH17 cytokines, which in turn may contribute to aging-associated chronic inflammation or "inflammaging." Of note, the antiaging drug metformin reverses this autophagy defect and rejuvenates CD4 T cell function.
巴拉特等人在 2020 年的报告中指出,衰老个体的 CD4 淋巴细胞存在线粒体自噬缺陷,导致氧化还原代谢改变和 TH17 细胞因子上调,而这反过来可能导致与衰老相关的慢性炎症或“炎症衰老”。值得注意的是,抗衰老药物二甲双胍可逆转这种自噬缺陷并恢复 CD4 T 细胞功能。