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New Insights into Mitochondria in Health and Diseases

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

Deadline for manuscript submissions: 20 May 2025 | Viewed by 710

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Department of Biology, Merrimack College, North Andover, MA 01845, USA
Interests: mitochondria; bioenergetic function; Warburg effect; mitochondria-targeted cancer chemotherapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Mitochondria are dynamic intracellular organelles that have long been considered the “powerhouses” of eukaryotic cells due to their central role in the process of aerobic metabolism. Research in the past two decades has revealed an ever-increasing number of new roles for mitochondria in the regulation of the life and death of the cell. For example, mitochondria are now known to be the main intracellular source of reactive oxygen species in most tissues and, as such, play an important role as signaling molecules that induce changes in cell proliferation, differentiation, and gene transcription. Mitochondria are also known to activate intrinsic apoptosis, an energy-dependent cell death pathway with a crucial function in normal tissue morphogenesis and homeostasis, tissue remodeling, and wound healing. More recently, mitochondria have been shown to play important roles in the immune response and in the aging process. Notably, mitochondrial DNA mutations and dysfunction have also been implicated as a causal or contributing factor in the development and/or progression of multiple diseases, including rare metabolic disorders such as Kearns–Sayre syndrome, Leigh’s disease, and mitochondrial myopathy, as well as some of the more common systemic diseases, such as diabetes, Parkinson’s disease, and cancer.

The purpose of this Special Issue is to highlight the many and varied roles that mitochondria play in the life and death of a cell, and to provide a forum for presenting new advances in our understanding of mitochondrial function in health maintenance and disease. The submission of reviews and basic or translational research articles is encouraged.

Dr. Josephine S. Modica-Napolitano
Guest Editor

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Keywords

  • mitochondrial bioenergetics
  • reactive oxygen species
  • apoptosis
  • aging
  • immune function
  • mtDNA mutations
  • mitochondrial dysfunction
  • mitochondria-targeted therapies

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Published Papers (1 paper)

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Research

12 pages, 3953 KiB  
Article
Sexual Dimorphism of Ethanol-Induced Mitochondrial Dynamics in Purkinje Cells
by Rehana Khatoon, Jordan Fick, Abosede Elesinnla, Jaylyn Waddell and Tibor Kristian
Int. J. Mol. Sci. 2024, 25(24), 13714; https://doi.org/10.3390/ijms252413714 (registering DOI) - 22 Dec 2024
Abstract
The cerebellum, a key target of ethanol’s toxic effects, is associated with ataxia following alcohol consumption. However, the impact of ethanol on Purkinje cell (PC) mitochondria remains unclear. To investigate how ethanol administration affects mitochondrial dynamics in cerebellar Purkinje cells, we employed a [...] Read more.
The cerebellum, a key target of ethanol’s toxic effects, is associated with ataxia following alcohol consumption. However, the impact of ethanol on Purkinje cell (PC) mitochondria remains unclear. To investigate how ethanol administration affects mitochondrial dynamics in cerebellar Purkinje cells, we employed a transgenic mouse model expressing mitochondria-targeted yellow fluorescent protein in Purkinje cells (PC-mito-eYFP). Both male and female PC-mito-eYFP mice received an intraperitoneal injection of ethanol or vehicle. One hour after ethanol administration, the animals were perfusion fixed or their cerebellum tissue or isolated mitochondria were collected. Cerebellum sections were analyzed using confocal microscopy to assess changes in mitochondrial length distribution. In vivo superoxide levels were measured using dihydroethidium (DHE), and mitochondrial NAD levels were determined by high-performance liquid chromatography (HPLC). Our findings revealed a sex-dependent response to ethanol administration in mitochondrial size distribution. While male Purkinje cell mitochondria exhibited no significant changes in size, female mitochondria became more fragmented after one hour of ethanol administration. This coincided with elevated phosphorylation of the fission protein Drp1 and increased superoxide production, as measured by DHE fluorescence intensity. Similarly, mitochondrial NAD levels were significantly reduced in female mice, but no changes were observed in males. Our results demonstrate that ethanol induced mitochondrial fragmentation through increased free radical levels, due to reduced NAD and increased p-Drp1, in PC cells of the female cerebellum. Full article
(This article belongs to the Special Issue New Insights into Mitochondria in Health and Diseases)
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