Autophagy is a fundamental cellular process discovered as a response to nutrient deprivation. It provides the cellular and molecular machinery for catabolism of cellular constituents, generating energy and providing building blocks for continued survival. However, autophagy does much more than provide an entry into catabolic pathways, it provides a mechanism for intracellular quality control, removing damaged organelles and misfolded proteins, processes critical for cellular health. Autophagy serves as a counterpoint to cell growth and anabolic events, activated when growth is not possible or is suppressed. Hence, there is an inherent antagonism between autophagy and growth. Heparan sulfate modified proteins are important co-receptors that generally promote growth factor activity and are therefore positioned within signaling networks that inhibit, or negatively regulate autophagy levels. This review summarizes evidence that heparan sulfate modified proteins provide an evolutionarily conserved inhibitory modulation of autophagy that can have profound effects on cell physiology and organismal responses to stress.

自噬是一种基本的细胞过程，被发现是对营养缺乏的反应。它为细胞成分的分解代谢提供细胞和分子机制，产生能量并为持续生存提供基石。然而，自噬不仅仅是提供进入分解代谢途径的途径，它还提供了一种细胞内质量控制机制，去除受损的细胞器和错误折叠的蛋白质，这些过程对细胞健康至关重要。自噬作为细胞生长和合成代谢事件的对位点，当生长不可能或被抑制时被激活。因此，自噬与生长之间存在固有的拮抗作用。硫酸乙酰肝素修饰蛋白是重要的共同受体，通常促进生长因子活性，因此位于抑制、或负调节自噬水平。这篇综述总结了硫酸乙酰肝素修饰蛋白提供了一种进化上保守的自噬抑制调节的证据，这种调节可以对细胞生理学和机体对压力的反应产生深远的影响。