ArticleiScience2024
Spastin regulates ER-mitochondrial contact sites and mitochondrial homeostasis.
Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Proteomic analysis reveals early pathological defects in corticospinal motor neurons of a spastin model of hereditary spastic paraplegia, which are improved by NU-9 treatment.Neurobiology of disease · 2026Article
- Mitochondria-ER contact sites in neurological disorders.Animal cells and systems · 2026Review
- Serendipitous Symptom Control: Allopurinol for Spasticity in a Case of SPG4-Linked Hereditary Spastic Paraplegia-A Case Report.Clinical case reports · 2026Article
- Piperine Enhances Mitochondrial Biogenesis to Mitigate Stress in SH-SY5Y Neuroblastoma Cells.Food science & nutrition · 2025Article
- Targeting MDM2 affects spastin protein levels and functions: implications for HSP treatment.Cell death discovery · 2025Article
- Rheumatoid arthritis-associated depression: focusing on the interactions between mitochondria and endoplasmic reticulum.Frontiers in pharmacology · 2025Review
- Approaches to Organelle Spacing at Membrane Contact Sites.Contact (Thousand Oaks (Ventura County, Calif.))Article
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria-endoplasmic reticulum (ER) contact sites (MERCs) emerged to play critical roles in numerous cellular processes, and their dysregulation has been associated to neurodegenerative disorders. Mutations in the SPG4 gene coding for spastin are among the main causes of hereditary spastic paraplegia (HSP). Spastin binds and severs microtubules, and the long isoform of this protein, namely M1, spans the outer leaflet of ER membrane where it interacts with other ER-HSP proteins. Here, we showed that overexpressed M1 spastin localizes in ER-mitochondria intersections and that endogenous spastin accumulates in MERCs. We demonstrated in different cellular models that downregulation of spastin enhances the number of MERCs, alters mitochondrial morphology, and impairs ER and mitochondrial calcium homeostasis. These effects are associated with reduced mitochondrial membrane potential, oxygen species levels, and oxidative metabolism. These findings extend our knowledge on the role of spastin in the ER and suggest MERCs deregulation as potential causes of SPG4-HSP disease.
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Registered trials
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