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Autophagy and Age-Associated Pathologies

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (31 December 2021) | Viewed by 2622

Special Issue Editor


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Guest Editor
Department of Biology, University of Rome Tor Vergata, Rome, Italy
Interests: autophagy; mitophagy; lysosome; neurodegenerative diseases; Alzheimer; rare genetic diseases; Down syndrome

Special Issue Information

Dear colleagues,

Autophagy and selective autophagy, such as mitophagy and ER-phagy, have been implicated in the development and progression of a growing number of diseases. Several studies have shown that autophagy is compromised with age and its dysregulation may significantly contribute to the development of age-associated pathologies, as it happens in Alzheimer’s disease or in many tumors. Many aspects of its role in the onset of several diseases have been clarified; however, many more questions remain unanswered, and often, its exact role in the process of neurodegenerative diseases is still under debate.

Thus, this Special Issue aims to review advances in the field of autophagy and its role in age-associated pathologies, including Alzheimer’s disease, Parkinson, amyotrophic lateral sclerosis, liver diseases, diabetes, metabolic diseases, and cancer, with the purpose of better characterizing the molecular dysregulations affecting the autophagic pathway that could underlie the development and progression of the disease.

Dr. Matteo Bordi
Guest Editor

Manuscript Submission Information

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Keywords

  • Autophagy
  • Mitophagy
  • Lysosome
  • Neurodegenerative diseases
  • Cancer
  • Oxidative stress
  • Mitochondrial metabolism
  • ER-phagy

Published Papers (1 paper)

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Research

13 pages, 2843 KiB  
Article
miR-302 Attenuates Mutant Huntingtin-Induced Cytotoxicity through Restoration of Autophagy and Insulin Sensitivity
by Ching-Chi Chang, Sing-Hua Tsou, Wei-Jen Chen, Ying-Jui Ho, Hui-Chih Hung, Guang-Yaw Liu, Sandeep Kumar Singh, Hsin-Hua Li and Chih-Li Lin
Int. J. Mol. Sci. 2021, 22(16), 8424; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22168424 - 05 Aug 2021
Cited by 9 | Viewed by 1966
Abstract
Huntington’s disease (HD) is an autosomal-dominant brain disorder caused by mutant huntingtin (mHtt). Although the detailed mechanisms remain unclear, the mutational expansion of polyglutamine in mHtt is proposed to induce protein aggregates and neuronal toxicity. Previous studies have shown that the decreased insulin [...] Read more.
Huntington’s disease (HD) is an autosomal-dominant brain disorder caused by mutant huntingtin (mHtt). Although the detailed mechanisms remain unclear, the mutational expansion of polyglutamine in mHtt is proposed to induce protein aggregates and neuronal toxicity. Previous studies have shown that the decreased insulin sensitivity is closely related to mHtt-associated impairments in HD patients. However, how mHtt interferes with insulin signaling in neurons is still unknown. In the present study, we used a HD cell model to demonstrate that the miR-302 cluster, an embryonic stem cell-specific polycistronic miRNA, is significantly downregulated in mHtt-Q74-overexpressing neuronal cells. On the contrary, restoration of miR-302 cluster was shown to attenuate mHtt-induced cytotoxicity by improving insulin sensitivity, leading to a reduction of mHtt aggregates through the enhancement of autophagy. In addition, miR-302 also promoted mitophagy and stimulated Sirt1/AMPK-PGC1α pathway thereby preserving mitochondrial function. Taken together, these results highlight the potential role of miR-302 cluster in neuronal cells, and provide a novel mechanism for mHtt-impaired insulin signaling in the pathogenesis of HD. Full article
(This article belongs to the Special Issue Autophagy and Age-Associated Pathologies)
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