Volume 21 Issue 12
Dec.  2023
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ZHANG Yi, WEI Na. FAM134B-mediated endoplasmic reticulum autophagy and its association with diseases[J]. Chinese Journal of General Practice, 2023, 21(12): 2114-2118. doi: 10.16766/j.cnki.issn.1674-4152.003303
Citation: ZHANG Yi, WEI Na. FAM134B-mediated endoplasmic reticulum autophagy and its association with diseases[J]. Chinese Journal of General Practice, 2023, 21(12): 2114-2118. doi: 10.16766/j.cnki.issn.1674-4152.003303

FAM134B-mediated endoplasmic reticulum autophagy and its association with diseases

doi: 10.16766/j.cnki.issn.1674-4152.003303
Funds:

 U1812403-6-1-6

 黔科合基础-ZK[2022]一般439

 FZSW-2021-007

  • Received Date: 2023-03-23
    Available Online: 2024-01-29
  • Autophagy has the ability to degrade damaged senescent organelles and abnormal proteins, providing energy and raw materials for life activities. Autophagy is mainly divided into four stages, including the formation of autophagic precursors, autophagosomes, autophagic lysosomes and the degradation of autophagic contents by lysosome hydrolase, which depends on the lysosomal degradation system. The endoplasmic reiculum (ER) is the largest organelle in eukaryotes, the site of protein synthesis and processing, and the storage site for calcium ions; protein folding errors and calcium ion imbalances lead to ER dysfunction and activate ER autophagy. Autophagy maintains cell homeostasis; selective and non-selective autophagy are two types of autophagy based on degraded substrate specificity. ER-phagy is a type of selective autophagy mediated by ER receptors. FAM134B is the first mammalian ER-phagy receptor to be identified, which mediates ER-phagy involved in the pathogenesis of all types of diseases. Family with sequence similarity 134, member B(FAM134B) induced the bending and fragmentation of the ER through the LC3 interaction domain and the reticular homologous domain, which facilitated transport to lysosomes and promoted the degradation of the ER. Moderate ER-phagy clears the damaged ER and restores ER homeostasis, whereas excessive ER-phagy induces apoptosis. In general, low levels of autophagy are beneficial for cell survival, whereas excessive autophagy or autophagy dysfunction under stress is detrimental. This paper introduces autophagy, ER structure and function, ER-phagy and how FAM134B mediates ER-phagy. By reviewing the relevant literatures, this paper explains the relationship between FAM134B-mediated ER-phagy and nervous system, digestive system, cardiovascular diseases and infectious diseases, and suggests that ER-phagy can be controlled by regulating the expression of FAM134B, thereby interfering with the progression of diseases.

     

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