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Cellular and Molecular Biology of Mitochondria in Human Health and Diseases

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: 10 July 2024 | Viewed by 1329

Special Issue Editor


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Guest Editor
Department of Regenerative Medicine, Kyoto Prefectural University of Medicine, 465 Kajii cho, Kamigyo ku, Kyoto 602-8655, Japan
Interests: mitochondrial biology; lysosomal biology; organelle; RNA decay; gene therapy
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Special Issue Information

Dear Colleagues,

Apart from being energy-producing plants, mitochondria regulate cell differentiation, play a major role in the initiation and progression of cancer, are responsible for cell death, serve as a command post for immunity, contribute to the maintenance of body temperature, play a key role in the external environment and intrinsic stress responses, and are so deeply involved in the aging process that they can be said to be involved in every process. The two life forms, which began in symbiosis, make up a single, brilliantly integrated organism. However, from time to time, we can glimpse the selfish behavior of the little one in the dysfunction of disease, and we know that it has a vigorous survival strategy. Biology has long been described by information reduced to genes encoded in the nucleus and has not given much significance to the malfunction of mitochondria, which were originally a separate life form. Recent advances in mitochondrial biology have revealed a series of events in which mitochondrial function responds to instructions from the nuclear genome, leading to alterations in the phenotype. In this special issue, we would like to provide an editorial on the understanding of diseases with pathologies based on mitochondrial dysfunction and the potential of new therapeutic strategies by correcting mitochondrial function. It would be a great pleasure for the editors to highlight the possibility of a common approach of restoring mitochondrial function to diseases with completely different etiologies, such as cancer, infectious diseases, neurodegenerative diseases, autoimmune diseases, and diabetes, by providing a cross-sectional overview from the perspective of mitochondria. To this end, we sincerely hope to receive papers from researchers focusing on mitochondria in a variety of fields.

Prof. Dr. Satoshi Gojo
Guest Editor

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Keywords

  • mitochondria
  • mitophagy
  • oxidative phosphorylation
  • apoptosis
  • integrated stress response
  • heteroplasmy
  • calcium dynamics
  • reactive oxygen species
  • fusion/fission
  • mitochondrial quality control

Published Papers (1 paper)

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Research

15 pages, 3250 KiB  
Article
Berberine Induces Mitophagy through Adenosine Monophosphate-Activated Protein Kinase and Ameliorates Mitochondrial Dysfunction in PINK1 Knockout Mouse Embryonic Fibroblasts
by Jee-Hyun Um, Kang-Min Lee, Young-Yeon Kim, Da-Ye Lee, Eunmi Kim, Dong-Hyun Kim and Jeanho Yun
Int. J. Mol. Sci. 2024, 25(1), 219; https://doi.org/10.3390/ijms25010219 - 22 Dec 2023
Cited by 1 | Viewed by 990
Abstract
Mitophagy stimulation has been shown to have a therapeutic effect on various neurodegenerative diseases. However, nontoxic mitophagy inducers are still very limited. In this study, we found that the natural alkaloid berberine exhibited mitophagy stimulation activity in various human cells. Berberine did not [...] Read more.
Mitophagy stimulation has been shown to have a therapeutic effect on various neurodegenerative diseases. However, nontoxic mitophagy inducers are still very limited. In this study, we found that the natural alkaloid berberine exhibited mitophagy stimulation activity in various human cells. Berberine did not interfere with mitochondrial function, unlike the well-known mitophagy inducer carbonyl cyanide m-chlorophenyl hydrazone (CCCP), and subsequently induced mitochondrial biogenesis. Berberine treatment induced the activation of adenosine monophosphate-activated protein kinase (AMPK), and the AMPK inhibitor compound C abolished berberine-induced mitophagy, suggesting that AMPK activation is essential for berberine-induced mitophagy. Notably, berberine treatment reversed mitochondrial dysfunction in PINK1 knockout mouse embryonic fibroblasts. Our results suggest that berberine is a mitophagy-specific inducer and can be used as a therapeutic treatment for neurodegenerative diseases, including Parkinson’s disease, and that natural alkaloids are potential sources of mitophagy inducers. Full article
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