Department of Medicine, Albert Einstein College of Medicine, Bronx, NY 10461, USA; Department of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Department of Medicine, Albert Einstein College of Medicine, Bronx, NY 10461, USA; Department of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, NY 10461, USA; Institute for Aging Research, Albert Einstein College of Medicine, Bronx, NY 10461, USA; Einstein-Mount Sinai Diabetes Research Center, Albert Einstein College of Medicine, Bronx, NY 10461, USA; The Fleischer Institute for Diabetes and Metabolism, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Cell Metab. 2019 Jan 8;29(1):4-6. doi: 10.1016/j.cmet.2018.12.010.
Autophagy prevents pancreatic β cell death during obesity, although the mechanism of autophagy activation in the β cell has remained elusive. In this issue of Cell Metabolism, King et al. (2018) show that intracellular complement component C3 interacts with autophagy protein ATG16L1 and protects against β cell death by stimulating autophagy.
自噬可防止肥胖期间的胰岛β细胞死亡，但其在β细胞中被激活的机制仍不清楚。在本期《细胞代谢》中，King 等人（2018）表明，细胞内补体成分 C3 与自噬蛋白 ATG16L1 相互作用，并通过刺激自噬来防止β细胞死亡。
