Selective autophagy as a therapeutic target for neurological diseases.
Weilin XuUmut OcakLiansheng GaoSheng TuCameron J LenahanJianmin ZhangAnwen ShaoPublished in: Cellular and molecular life sciences : CMLS (2020)
The neurological diseases primarily include acute injuries, chronic neurodegeneration, and others (e.g., infectious diseases of the central nervous system). Autophagy is a housekeeping process responsible for the bulk degradation of misfolded protein aggregates and damaged organelles through the lysosomal machinery. Recent studies have suggested that autophagy, particularly selective autophagy, such as mitophagy, pexophagy, ER-phagy, ribophagy, lipophagy, etc., is closely implicated in neurological diseases. These forms of selective autophagy are controlled by a group of important proteins, including PTEN-induced kinase 1 (PINK1), Parkin, p62, optineurin (OPTN), neighbor of BRCA1 gene 1 (NBR1), and nuclear fragile X mental retardation-interacting protein 1 (NUFIP1). This review highlights the characteristics and underlying mechanisms of different types of selective autophagy, and their implications in various forms of neurological diseases.
Keyphrases
- cell death
- endoplasmic reticulum stress
- signaling pathway
- oxidative stress
- infectious diseases
- drug induced
- cell proliferation
- liver failure
- pi k akt
- amino acid
- endothelial cells
- binding protein
- protein kinase
- blood brain barrier
- dna methylation
- high glucose
- copy number
- stress induced
- respiratory failure
- cerebrospinal fluid