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Biomedicines
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Central Role of Mitochondrial Oxidative Stress in the Pathophysiology of...
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Central Role of Mitochondrial Oxidative Stress in the Pathophysiology of Disorders (2nd Edition)

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: 31 March 2026 | Viewed by 767

Special Issue Editors

Dr. Guilhian Leipnitz

E-Mail Website
Guest Editor
Department of Biochemistry, Universidade Federal do Rio Grande do Sul, Porto Alegre CEP 90035-903, Brazil
Interests: oxidative stress
Special Issues, Collections and Topics in MDPI journals
Dr. André Quincozes-Santos

E-Mail Website
Guest Editor
Departamento de Bioquímica, Universidade Federal do Rio, Grande do Sul, Rua Ramiro Barcelos, 2600-Anexo, Bairro Santa Cecília, Porto Alegre 90035-003, RS, Brazil
Interests: oxidative stress; glial cells; neuroprotection

Special Issue Information

Dear Colleagues,

Mitochondria are the main sites of cellular oxidation and energy conversion, and most cellular ATP is produced by oxidative phosphorylation. During oxidative phosphorylation, reactive oxygen species (ROS) are produced as byproducts in mitochondria, primarily by the respiratory chain complexes I and III, and are sequestered by antioxidant defenses. Mitochondrial functionality is also maintained by the so-called mitochondrial quality control, which includes processes such as mitochondrial biogenesis, dynamics, and mitophagy. Since mitochondria are considered the main source of reactive oxygen species (ROS) production in cells, impairments in bioenergetics or any mitochondrial quality control process are often accompanied by elevated ROS and oxidative damage. Therefore, mitochondrial dysfunction and ROS production are involved in the pathophysiology of primary mitochondrial diseases, neurodegenerative disorders, cardiac insufficiency, diabetes mellitus, and aging, among others. Antioxidants and modulators of mitochondrial function can reduce mitochondrial oxidative damage and are considered promising therapeutic strategies for these pathologies. In this Special Issue, we aim to contribute to a better understanding of the pathophysiology of different pathologies characterized by mitochondrial dysfunction and reveal novel therapeutic approaches for these disorders. We look forward to your contributions to this Special Issue.

Dr. Guilhian Leipnitz
Dr. André Quincozes-Santos
Guest Editors

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Keywords

  • mitochondrial dysfunction
  • reactive oxygen species
  • bioenergetics
  • mitochondrial quality control
  • pathologies
  • protective agents

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Published Papers (1 paper)

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Research

36 pages, 19130 KB  
Article
The Transgenerational Impact of High-Fat Diet and Diabetic Pregnancy on Embryonic Transcriptomics and Mitochondrial Health
by Abigail K. Klein, Benjamin P. Derenge, Malini Mukherjee, Srikrishna P. Reddy, Tricia D. Larsen, Prathapan Ayyappan, Tyler C. T. Gandy, Kyle M. Siemers, Michael S. Kareta and Michelle L. Baack
Biomedicines 2025, 13(8), 2019; https://doi.org/10.3390/biomedicines13082019 - 19 Aug 2025
Viewed by 567
Abstract
Background/Objectives: Overnutrition increases comorbidities such as gestational diabetes during pregnancy that can have detrimental consequences for both parent and progeny. We previously reported that high-fat (HF) diet and late-gestation diabetes (DM) incite mitochondrial dysfunction, oxidative stress, and cardiometabolic disease in first generation (F1) [...] Read more.
Background/Objectives: Overnutrition increases comorbidities such as gestational diabetes during pregnancy that can have detrimental consequences for both parent and progeny. We previously reported that high-fat (HF) diet and late-gestation diabetes (DM) incite mitochondrial dysfunction, oxidative stress, and cardiometabolic disease in first generation (F1) rat offspring, partially through epigenomic and transcriptomic programming. Primordial germ cells, which become the second generation (F2), are also exposed, which could incite generational risk. This study aimed to determine whether the F2 transcriptome already has genomic variation at the preimplantation embryo stage, and whether variations normalize, persist or compound in the third generation (F3). Methods: F0 female rats were fed a control or HF diet, then DM was induced in HF-fed dams on gestational day (GD)14, exposing F1 offspring and F2 primordial germ cells to hyperlipidemia, hyperglycemia and fetal hyperinsulinemia during the last third of pregnancy. F1 pups were reared by healthy dams and bred to produce F2 embryos (F2e) and F2 pups. F2 offspring were bred to produce F3 embryos (F3e). Embryos were assessed by a novel grading method, live cell imaging, and single-cell RNA sequencing. Results: Embryo grades were not different, but HF+DM F2e had more cells while F3e had fewer cells and overall fewer embryos. HF+DM F2e had similar mitochondria quantity but a downregulation of genes involved in lipid metabolism and more oxidative stress, consistent with mitochondrial dysfunction. They also had an upregulation of chromatin-remodeling genes. The predicted developmental effect is accelerated embryo aging and epigenetic drift. In contrast, HF+DM F3e had an adaptive stress response leading to increased mitochondria quantity and an upregulation of genes involved in mitochondrial respiration, metabolism, and genomic repair that led to a predicted developmental effect of delayed embryo maturation. Conclusions: Although pathways vary, both generations have metabolically linked differentially expressed genes that influence cell fate and developmental pathways. In conclusion, HF+DM pregnancy can program the early embryonic transcriptome for three generations, despite an intergenerational healthy diet. Full article
(This article belongs to the Special Issue Central Role of Mitochondrial Oxidative Stress in the Pathophysiology of Disorders (2nd Edition))
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