Specific membrane lipids play unique roles in (macro)autophagy. Those include phosphatidylethanolamine, to which LC3/GABARAP autophagy proteins become covalently bound in the process, or cardiolipin, an important effector in mitochondrial autophagy (or mitophagy). Ceramide (Cer), or N-acyl sphingosine, is one of the simplest sphingolipids, known as a stress signal in the apoptotic pathway. Moreover, Cer is increasingly being recognized as an autophagy activator, although its mechanism of action is unclear. In the present review, the proposed Cer roles in autophagy are summarized, together with some biophysical properties of Cer in membranes. Possible pathways for Cer activation of autophagy are discussed, including specific protein binding of the lipid, and Cer-dependent perturbation of bilayer properties. Cer generation of lateral inhomogeneities (domain formation) is given special attention. Recent biophysical results, including fluorescence and atomic force microscopy data, show Cer-promoted enhanced binding of LC3/GABARAP to lipid bilayers. These observations could be interpreted in terms of the putative formation of Cer-rich nanodomains.

特定的膜脂在（宏观）自噬中发挥独特的作用。其中包括磷脂酰乙醇胺（LC3/GABARAP自噬蛋白在此过程中与其共价结合）或心磷脂（线粒体自噬（或线粒体自噬）中的重要效应物）。神经酰胺 (Cer) 或 N-酰基鞘氨醇是最简单的鞘脂之一，被称为细胞凋亡途径中的应激信号。此外，Cer 越来越被认为是一种自噬激活剂，尽管其作用机制尚不清楚。在本综述中，总结了所提出的 Cer 在自噬中的作用，以及膜中 Cer 的一些生物物理特性。讨论了 Cer 激活自噬的可能途径，包括脂质的特异性蛋白质结合，以及双层特性的 Cer 依赖性扰动。横向不均匀性（区域形成）的产生受到特别关注。最近的生物物理结果，包括荧光和原子力显微镜数据，表明 Cer 促进了 LC3/GABARAP 与脂质双层的结合增强。这些观察结果可以用富含 Cer 的纳米域的假定形成来解释。