Correction for Lee et al., Altered ER–mitochondria contact impacts mitochondria calcium homeostasis and contributes to neurodegeneration in vivo in disease models

doi:10.1073/pnas.1815900115

Cited by 2 publications

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“…The recruitment and perturbation of the ER network might contribute to cytotoxicity during inclusion formation, but on its own does not appear to be sufficient to cause overt toxicity. Consistent with this hypothesis, the ERAD and Ca 2+ signaling pathways have been extensively reported to be dysregulated in various cellular and animal models using different Htt fragments [132][133][134][135][136][137] .…”

Section: Cytoplasmic Httex1 Inclusion Formation and Maturation Involves A Complex Interplay Between Httex1 Aggregates And Organellesmentioning

confidence: 59%

Nuclear and cytoplasmic huntingtin inclusions exhibit distinct biochemical composition, interactome and ultrastructural properties

Riguet

Mahul‐Mellier

Maharjan

et al. 2020

Preprint

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Despite the strong evidence linking the aggregation of the Huntingtin protein (Htt) to the pathogenesis of Huntington’s disease (HD), the mechanisms underlying Htt aggregation and neurodegeneration remain poorly understood. Herein, we investigated the ultrastructural properties and protein composition of Htt inclusions in cells overexpressing mutant exon1 of the Htt protein. Our findings provide novel insight into the ultrastructural properties of cytoplasmic and nuclear Htt inclusions and their mechanisms of formation. We show that Htt inclusion formation and maturation are complex processes that, although initially driven by polyQ-dependent Htt aggregation, also involve 1) polyQ and PRD domain-dependent sequestration of lipids and cytoplasmic and cytoskeletal proteins related to HD dysregulated pathways; 2) recruitment and accumulation of remodeled or dysfunctional membranous organelles; and 3) impairement of the protein quality control and degradation machineries. Interestingly, nuclear and cytoplasmic Htt inclusions exhibited distinct biochemical composition and ultrastructural properties, suggesting different formation mechanisms and toxicity.Graphical AbstractSchematic depictions and original electron micrographs of cytoplasmic inclusions formed by native (tag-free) mutant Huntington exon1 proteins (Httex1 72Q, left) and the corresponding GFP fusion protein (Httex1 72Q-GFP).

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Section: Cytoplasmic Httex1 Inclusion Formation and Maturation Involves A Complex Interplay Between Httex1 Aggregates And Organellesmentioning

confidence: 59%

Nuclear and cytoplasmic huntingtin inclusions exhibit distinct biochemical composition, interactome and ultrastructural properties

Riguet

Mahul‐Mellier

Maharjan

et al. 2020

Preprint

View full text Add to dashboard Cite

show abstract

Mitophagy and its regulatory mechanisms in the biological effects of nanomaterials

Zhang,

Yang,

Guo

et al. 2024

J of Applied Toxicology

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Mitophagy is a selective cellular process critical for the removal of damaged mitochondria. It is essential in regulating mitochondrial number, ensuring mitochondrial functionality, and maintaining cellular equilibrium, ultimately influencing cell destiny. Numerous pathologies, such as neurodegenerative diseases, cardiovascular disorders, cancers, and various other conditions, are associated with mitochondrial dysfunctions. Thus, a detailed exploration of the regulatory mechanisms of mitophagy is pivotal for enhancing our understanding and for the discovery of novel preventive and therapeutic options for these diseases. Nanomaterials have become integral in biomedicine and various other sectors, offering advanced solutions for medical uses including biological imaging, drug delivery, and disease diagnostics and therapy. Mitophagy is vital in managing the cellular effects elicited by nanomaterials. This review provides a comprehensive analysis of the molecular mechanisms underpinning mitophagy, underscoring its significant influence on the biological responses of cells to nanomaterials. Nanoparticles can initiate mitophagy via various pathways, among which the PINK1‐Parkin pathway is critical for cellular defense against nanomaterial‐induced damage by promoting mitophagy. The role of mitophagy in biological effects was induced by nanomaterials, which are associated with alterations in Ca2+ levels, the production of reactive oxygen species, endoplasmic reticulum stress, and lysosomal damage.

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Correction for Lee et al., Altered ER–mitochondria contact impacts mitochondria calcium homeostasis and contributes to neurodegeneration in vivo in disease models

Cited by 2 publications

References 0 publications

Nuclear and cytoplasmic huntingtin inclusions exhibit distinct biochemical composition, interactome and ultrastructural properties

Nuclear and cytoplasmic huntingtin inclusions exhibit distinct biochemical composition, interactome and ultrastructural properties

Mitophagy and its regulatory mechanisms in the biological effects of nanomaterials

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