Mitochondrial Dynamics and Function

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Cell Biology".

Deadline for manuscript submissions: closed (15 May 2023) | Viewed by 2390

Special Issue Editors


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Guest Editor
Key Laboratory of Applied Technology on Green-Eco-Healthy Animal Husbandry of Zhejiang Province, College of Animal Science and Technology, College of Veterinary Medicine, Zhejiang A&F University, Hangzhou 311300, China
Interests: mitochondria; oxidative stress; autophagy; apoptosis; inflammation; mitochondrial disease

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Guest Editor
Institute of Animal Science, Jiangsu Academy of Agricultural Sciences, Nanjing 210014, China
Interests: heat stress; mitochondria; oxidative stress; autophagy; apoptosis
Department of Biomedical Engineering, SUNY at Binghamton, Binghamton, NY 13902-6000, USA
Interests: mathematical biology; mitochondria and cytoskeleton interaction; mechanobiology; mitochondria dynamics; electrophysiology; computational physics

Special Issue Information

Dear Colleagues,

Mitochondria are highly dynamic organelles that constantly undergo fission and fusion events, referred to as mitochondrial dynamics, to maintain their shape, number and size, as well as subcellular distribution. Mitochondrial fission allows the division of one mitochondrion into two daughter mitochondria by recruiting dynamin-related protein, whereas mitochondrial fusion is the union of two mitochondria resulting in one mitochondria by coordinating mitofusin1/2 and optic atrophy 1 (OPA1). Mitochondrial dynamics is associated with various cellular processes, including cell cycle, cell metabolism, apoptosis, mitophagy, cell proliferation and reactive oxygen species (ROS) production. Mitochondrial fission is critical for mitophagy to remove the misfolded proteins or mutated DNA from mitochondria, abnormal fission and mitophagy could induce the accumulation of dysfunctional mitochondria in cells. Defects in mitochondrial dynamics are correlated with many human diseases, including cancer, neurodegenerative disease, aging and infertility. Thus, regulators of mitochondrial homeostasis, biogenesis and function have evolved as promising novel targets for the treatment of mitochondrial dysfunction-associated diseases.

This Special Issue aims to collect original research and review articles to understand the physiological, metabolic, and cellular mechanisms that characterize the interaction between mitochondrial regulatory factors and the occurrence of diseases.

Prof. Dr. Xing Duan
Dr. Kun-Lin Chen
Dr. Yizeng Li
Guest Editors

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Keywords

  • mitochondrial function
  • oxidative stress
  • autophagy
  • apoptosis
  • aging
  • obesity
  • diabetes mellitus
  • infertility
  • cancer

Published Papers (1 paper)

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Research

14 pages, 3287 KiB  
Article
Mitochondrial Dysfunction in CD4+ T Effector Memory RA+ Cells
by Marie Strickland, Salanne Lee, Shi Yong Neo, Akhila Balachander, Ivy Low, Seri Mustafah, Wah Ing Goh, Graham D. Wright, Anis Larbi and Sylvia L. F. Pender
Biology 2023, 12(4), 597; https://doi.org/10.3390/biology12040597 - 14 Apr 2023
Cited by 4 | Viewed by 1921
Abstract
Human ageing is accompanied by poor responses to infection and decreased vaccine efficacy. While the causes of this can be attributed to defects in the immune system that increase with age, it is unknown whether mitochondrial dysfunction may also contribute to these phenomena. [...] Read more.
Human ageing is accompanied by poor responses to infection and decreased vaccine efficacy. While the causes of this can be attributed to defects in the immune system that increase with age, it is unknown whether mitochondrial dysfunction may also contribute to these phenomena. This study aims to assess mitochondrial dysfunction in CD4+ terminal effector memory T cells re-expressing CD45RA (TEMRA) cells and other CD4+ memory T cell subtypes, which are increased in number in the elderly population, with respect to how their metabolic responses to stimulation are altered compared to CD4+ naïve T cells. In this study, we show that CD4+ TEMRA cells exhibit altered mitochondrial dynamics compared to CD4+ naïve cells and CD4+ central and effector memory cells, with a 25% reduction in OPA1 expression. CD4+ TEMRA and memory cells show increased upregulation of Glucose transporter 1 following stimulation and higher levels of mitochondrial mass compared to CD4+ naïve T cells. Additionally, TEMRA cells exhibit a decrease in mitochondrial membrane potential compared to other CD4+ memory cell subsets by up to 50%. By comparing young to aged individuals, more significant mitochondria mass and lower membrane potential were observed in CD4+ TEMRA of young individuals. In conclusion, we suggest that CD4+ TEMRA cells may be impaired with respect to their metabolic response to stimulation, possibly contributing to impaired responses to infection and vaccination. Full article
(This article belongs to the Special Issue Mitochondrial Dynamics and Function)
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