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Special Issue "Autophagy in Health, Aging and Disease 4.0"

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Dear Colleagues,

Autophagy is an evolutionarily conserved intracellular catabolic process. It has an essential role in cellular homeostasis, facilitating lysosomal degradation and the recycling of harmful and damaged cytoplasmic components. Autophagy was first discovered as a survival mechanism in yeasts subjected to nutrient deprivation, and since then, studies in several different organisms have established its critical roles in a variety of biological processes ranging from development to aging. Interestingly, autophagy is often found perturbed in age-related disorders such as cancer, diabetes, neurodegenerative diseases, and sarcopenia. Accordingly, autophagy is important for the maintenance of organismal health, which prominently declines with aging.

This Special Issue of the International Journal of Molecular Sciences, “Autophagy in Health, Aging and Disease 4.0”, will include a selection of original articles and reviews aimed at expanding our understanding of this multifaceted process and providing support for further investigations on the role of autophagy in cellular homeostasis, aging, and disease. In particular, it will contribute to better explaining the complex machinery of autophagy and lead to further investigations on physiological and pathological fields in which the study of this process is still in its infancy. Moreover, studies on the role of autophagy in age-related processes to open new avenues for the development of novel potential anti-aging therapeutic approaches are also welcome.

Prof. Dr. Mirko Pesce
Prof. Dr. Antonia Patruno
Dr. Maccarone Rita
Guest Editors

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Keywords

autophagy
aging
aging diseases
cell survival
inflammation
oxidative stress
signaling pathway
target identification

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Open AccessArticle

Altered Expression of Autophagy Biomarkers in Hippocampal Neurons in a Multiple Sclerosis Animal Model

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Int. J. Mol. Sci. 2023, 24(17), 13225; https://doi.org/10.3390/ijms241713225 - 25 Aug 2023

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Abstract

Multiple Sclerosis (MS) is a chronic inflammatory disease that affects the brain and spinal cord. Inflammation, demyelination, synaptic alteration, and neuronal loss are hallmarks detectable in MS. Experimental autoimmune encephalomyelitis (EAE) is an animal model widely used to study pathogenic aspects of MS. Autophagy is a process that maintains cell homeostasis by removing abnormal organelles and damaged proteins and is involved both in protective and detrimental effects that have been seen in a variety of human diseases, such as cancer, neurodegenerative diseases, inflammation, and metabolic disorders. This study is aimed at investigating the autophagy signaling pathway through the analysis of the main autophagic proteins including Beclin-1, microtubule-associated protein light chain (LC3, autophagosome marker), and p62 also called sequestosome1 (SQSTM1, substrate of autophagy-mediated degradation) in the hippocampus of EAE-affected mice. The expression levels of Beclin-1, LC3, and p62 and the Akt/mTOR pathway were examined by Western blot experiments. In EAE mice, compared to control animals, significant reductions of expression levels were detectable for Beclin-1 and LC3 II (indicating the reduction of autophagosomes), and p62 (suggesting that autophagic flux increased). In parallel, molecular analysis detected the deregulation of the Akt/mTOR signaling. Immunofluorescence double-labeling images showed co-localization of NeuN (neuronal nuclear marker) and Beclin-1, LC3, and p62 throughout the CA1 and CA3 hippocampal subfields. Taken together, these data demonstrate that activation of autophagy occurs in the neurons of the hippocampus in this experimental model. Full article

(This article belongs to the Special Issue Autophagy in Health, Aging and Disease 4.0)

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Special Issue "Autophagy in Health, Aging and Disease 4.0"

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