Palma Alessandro, Reggio Alessio
Department of Biology and Biotechnologies "Charles Darwin", Sapienza University of Rome, Rome, Italy.
Saint Camillus International University of Health Sciences, Rome, Italy.
J Cell Physiol. 2025 Jan;240(1):e31492. doi: 10.1002/jcp.31492. Epub 2024 Nov 25.
The endoplasmic reticulum (ER) is a pivotal organelle responsible for protein and lipid synthesis, calcium homeostasis, and protein quality control within eukaryotic cells. To maintain cellular health, damaged or excess portions of the ER must be selectively degraded via a process known as selective autophagy, or ER-phagy. This specificity is driven by a network of protein receptors and regulatory mechanisms. In this review, we explore the molecular mechanisms governing ER-phagy, with a focus on the FAM134 family of ER-resident ER-phagy receptors. We discuss the molecular pathways and Posttranslational modifications that regulate receptor activation and clustering, and how these modifications fine-tune ER-phagy in response to stress. This review provides a concise understanding of how ER-phagy contributes to cellular homeostasis and highlights the need for further studies in models where ER stress and autophagy are dysregulated.
内质网（ER）是一种关键的细胞器，负责真核细胞内的蛋白质和脂质合成、钙稳态以及蛋白质质量控制。为维持细胞健康，内质网受损或多余的部分必须通过一种称为选择性自噬或内质网自噬的过程进行选择性降解。这种特异性由蛋白质受体和调节机制网络驱动。在本综述中，我们探讨了内质网自噬的分子机制，重点关注内质网驻留的内质网自噬受体FAM134家族。我们讨论了调节受体激活和聚集的分子途径及翻译后修饰，以及这些修饰如何在应激反应中微调内质网自噬。本综述简要介绍了内质网自噬如何促进细胞稳态，并强调了在应激和自噬失调模型中进一步研究的必要性。
