autophagy

Autophagy is central to the pathogenesis of neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis.

Critical questions remain about autophagy in neurodegenerative disease despite progress in understanding its role.

Cell-type-specific autophagy regulation, interactions with other cellular pathways, and translation of autophagy-modulating therapies to clinical practice are pressing issues in the field.

Addressing unresolved questions about autophagy in neurodegenerative disease is expected to advance understanding and enable novel therapeutics.

Elucidating the autophagy regulatory network provides a foundation for designing next-generation crops that maintain high yield and resilience under climate-driven stress.

To develop effective anti-cancer therapy, the influence of tested compounds should be assessed on cell cycle, epithelial-mesenchymal transition, autophagy, and apoptosis.

Autophagy has a dichotomous role in mycobacterial infection, acting as a protective host mechanism while also being hijacked as a virulence determinant for bacterial survival.

Autophagy is essential for maintaining cellular homeostasis and enhancing plant resilience to multiple abiotic stresses.

Mycobacteria have evolved strategies to subvert or exploit autophagy for survival.

Autophagy serves as a host defense mechanism against mycobacteria by delivering bacteria to the lysosome.

Autophagy contributes to organellar quality control, metabolic adaptation, and stress-specific responses under diverse abiotic stresses.

Autophagy is recognized as a central regulator of stress signaling, hormonal crosstalk, and metabolic reprogramming in plants under abiotic stress.

Enhancing autophagy is presented as a route toward host-directed therapies against mycobacterial pathogens.

Mutations in genes encoding essential autophagy factors impair autophagy and are linked to ALS.

The mechanistic basis of autophagy-mediated neuroprotection, neuronal resistance to autophagy induction, and neuron-specific effects of autophagy-impairing mutations remains incompletely defined.

Autophagy is important for preventing and counteracting pathogenic insults that can lead to neurodegeneration.

The review covers critical autophagy steps, ALS-mutated factors that impair autophagy, their effects in disease models, and cell type-specific regulation in non-neuronal cells relevant to neurodegeneration.

Autophagy and the ubiquitin-proteasome system are the two major quality control pathways responsible for cellular homeostasis.

Autophagy and the ubiquitin-proteasome system intersect and communicate at multiple points to coordinate proteostasis and organelle homeostasis.

Autophagy and the ubiquitin-proteasome system protect against age-associated changes and many human diseases.

Ubiquitination serves as a degradation signal for both autophagy and the ubiquitin-proteasome system, but it is used differently by the two pathways.

Common principles and communication nodes linking autophagy and the ubiquitin-proteasome system may be therapeutically exploited.

Aberrant autophagy is implicated in toxin-induced parkinsonism and dopaminergic neurodegeneration leading to Parkinson's disease.

Autophagy and the ubiquitin proteasome system jointly support homeostasis of tyrosine hydroxylase-positive neurons through biodegradation of sub-cellular components.

Autophagy degrades aggregated proteins and impaired mitochondria in nigrostriatal dopaminergic neurons, including proteins such as α-synuclein, Parkin, and ubiquitin.

The review evaluates whether targeting defective autophagy could restore normal dopaminergic neuron function and potentially rescue Parkinson's disease pathogenesis.

Autophagy has both antiviral and proviral roles in virus-host interactions.

Autophagy is described as an essential component of host defense against viral infection.

Autophagy contributes to antiviral defense through xenophagy, innate immune signaling, and aspects of adaptive immunity.

Viruses have evolved strategies to evade autophagic attack and to manipulate autophagy machinery for their own benefit.

The review covers autophagy-related roles in antigen presentation, including MHC class II presentation of intracellular material.

The review covers LC3-associated phagocytosis as a non-canonical autophagy-protein-dependent pathway relevant to immunity and inflammatory control.

The review covers xenophagy as an autophagy-related mechanism for microbial clearance in immunity.

This review synthesizes evidence that autophagy intersects with host defense, inflammatory control, microbial clearance, antigen presentation, and disease-linked immune phenotypes.

Autophagic dysfunction is associated with cancer, neurodegeneration, microbial infection, and ageing.

Autophagy is a cellular pathway involved in protein and organelle degradation.

Autophagy is primarily protective for the cell but can also play a role in cell death.

Understanding autophagy may allow scientists and clinicians to harness this process to improve human health.

Expression of a regulatory HsAtg4 mutant prevented autophagosome formation in cells.

Starvation stimulates formation of reactive oxygen species, specifically H2O2, during starvation-induced autophagy.

Oxidative conditions are essential for autophagy because antioxidative treatment abolished autophagosome formation and protein degradation.