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Mitophagy in Neurodegeneration and Aging

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

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 2333

Special Issue Editors


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Guest Editor
1. Department Bioquímica y Biología Molecular y Genética, Facultad de Enfermería y Terapia Ocupacional, Universidad de Extremadura Avda de la Universidad S/N, 10003 Cáceres, Spain
2. Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), 28049 Madrid, Spain
3. Instituto Universitario de Investigación Biosanitaria de Extremadura (INUBE), 10003 Cáceres, Spain
Interests: autophagy; mitophagy; neurodegeneration; cell death; aging

E-Mail Website
Guest Editor
1. Department Bioquímica y Biología Molecular y Genética, Facultad de Enfermería y Terapia Ocupacional, Universidad de Extremadura Avda de la Universidad S/N, 10003 Cáceres, Spain
2. Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), 28049 Madrid, Spain
3. Instituto Universitario de Investigación Biosanitaria de Extremadura (INUBE), 10003 Cáceres, Spain
Interests: autophagy; mitophagy; neurodegeneration; repeat expansion diseases

E-Mail Website
Guest Editor
1. Department Bioquímica y Biología Molecular y Genética, Facultad de Enfermería y Terapia Ocupacional, Universidad de Extremadura Avda de la Universidad s/n, 10003 Cáceres, Spain
2. Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), 28049 Madrid, Spain
3. Instituto Universitario de Investigación Biosanitaria de Extremadura (INUBE), 10003 Cáceres, Spain
Interests: mitochondria; mitophagy; mlkl; necroptosis; rip; rotenone; mitochondrial; animal model

Special Issue Information

Dear Colleagues,

We are organizing a Special Issue of the International Journal of Molecular Sciences entitled “Mitophagy in Neurodegeneration and Aging”.

Mitochondria are organelles involved in crucial cellular processes, including the production of energy, lipid metabolism, or ion homeostasis. They also play key roles in the mechanisms of cell death and the generation of reactive oxygen species. Mitochondria are dynamic organelles that are continuously recycled through processes of biogenesis and degradation. Both processes must be balanced to maintain normal mitochondrial function.

Mitophagy is a type of selective autophagy that exclusively degrades damaged mitochondria or parts of them. Specifically, mitophagy is necessary to restore the mitochondrial steady state, regulating the mitochondrial population based on the metabolic demand or removing damaged mitochondria. Regarding this, failure of this mechanism can lead to neurodegeneration and aging. Strategies aimed at re-establishing these alterations could have beneficial effects. The goal of this Special Issue is, therefore, to highlight the role of mitophagy in chronic diseases such as neurodegenerative diseases and processes related to pathological aging. Here, we compile original manuscripts and review articles from outstanding experts in this field, covering the current state-of-the-art on the involvement of this catabolic process in the neurodegenerative and aging processes. Contributions that outline and review the key questions that still remain regarding the molecular mechanisms of mitophagy leading to the pathological course of these processes, as well as the translational applications of mitophagy-inducing compounds, are very welcome.

Dr. Rosa A. Gonzalez-Polo
Dr. Patricia Gomez-Suaga
Dr. Mireia Niso-Santano
Guest Editors

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Keywords

  • mitochondria
  • neurodegeneration
  • mitophagy
  • aging
  • cell death

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Published Papers (1 paper)

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Research

19 pages, 3280 KiB  
Article
Melatonin Attenuates H2O2-Induced Oxidative Injury by Upregulating LncRNA NEAT1 in HT22 Hippocampal Cells
by Qiang Gao, Chi Zhang, Jiaxin Li, Han Xu, Xiaocheng Guo, Qi Guo, Chen Zhao, Haixu Yao, Yuhan Jia and Hui Zhu
Int. J. Mol. Sci. 2022, 23(21), 12891; https://doi.org/10.3390/ijms232112891 - 25 Oct 2022
Cited by 4 | Viewed by 1823
Abstract
More research is required to understand how melatonin protects neurons. The study aimed to find out if and how long non-coding RNA (lncRNA) contributes to melatonin’s ability to defend the hippocampus from H2O2-induced oxidative injury. LncRNAs related to oxidative [...] Read more.
More research is required to understand how melatonin protects neurons. The study aimed to find out if and how long non-coding RNA (lncRNA) contributes to melatonin’s ability to defend the hippocampus from H2O2-induced oxidative injury. LncRNAs related to oxidative injury were predicted by bioinformatics methods. Mouse hippocampus-derived neuronal HT22 cells were treated with H2O2 with or without melatonin. Viability and apoptosis were detected by Cell Counting Kit-8 and Hoechst33258. RNA and protein levels were measured by quantitative real-time PCR, Western blot, and immunofluorescence. Bioinformatics predicted that 38 lncRNAs were associated with oxidative injury in mouse neurons. LncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) was related to H2O2-induced oxidative injury and up-regulated by melatonin in HT22 cells. The knockdown of NEAT1 exacerbated H2O2-induced oxidative injury, weakened the moderating effect of melatonin, and abolished the increasing effect of melatonin on the mRNA and protein level of Slc38a2. Taken together, melatonin attenuates H2O2-induced oxidative injury by upregulating lncRNA NEAT1, which is essential for melatonin stabilizing the mRNA and protein level of Slc38a2 for the survival of HT22 cells. The research may assist in the treatment of oxidative injury-induced hippocampal degeneration associated with aging using melatonin and its target lncRNA NEAT1. Full article
(This article belongs to the Special Issue Mitophagy in Neurodegeneration and Aging)
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