
Jan Jezek
University of Cambridge, Department of Genetics; Wellcome Trust/Cancer Research UK Gurdon Institute
<p>Dr. Jezek is a postdoctoral fellow at The Gurdon Institute, University of Cambridge, UK. His major is Biochemistry. His research interests are mitochondrial and redox biology, cancer research, tumor suppressors, mitochondrial stress signaling, mitochondrial dynamics, reactive oxygen species, apoptosis, hypoxia, transcriptional cyclins, mitochondrial DNA inheritance, mitochondrial recombination, mitochondrial DNA polymerase gamma, cytochrome c oxidase, germline development, and Drosophila genetics. He is a co-author of twenty-one articles in peer-reviewed international journals and a member of The Genetics Society, British Society for Cell Biology, and The Biochemical Society. He serves as an editorial board member in Biomedicines and Acta Scientific Cancer Biology.</p>

Vijay Menon
Yale University, Department of Therapeutic Radiology
<p>Dr. Vijay Menon is an Associate Research Scientist in the Department of Therapeutic Radiology at Yale University. His current work involves the study of UV-induced rare mutations in sun-exposed skin using high-throughput duplex sequencing to be used as a metric to measure a patient’s past UV exposure and future skin cancer risk. Dr. Menon received his PhD in Pharmacology and Toxicology from Virginia Commonwealth University (VCU) in Richmond, Virginia, during which he investigated the mechanism of action of novel platinum compounds in cancer cells. This was followed by postdoctoral positions at VCU and Icahn School of Medicine. His research expertise mainly includes DNA damage response and repair pathways, erythropoiesis and hematopoiesis, mitochondrial dynamics and redox signaling, and Next Generation Sequencing (NGS).</p>
Mitochondria play a fundamental role in cellular homeostasis by integrating energy production, metabolic signaling, redox balance, and cell fate decisions. Changes in mitochondrial morphology and function are increasingly recognized as active drivers—rather than passive consequences—of physiological adaptation and disease progression. Dysregulated mitochondrial dynamics, impaired bioenergetics, and defective quality control mechanisms have been linked to a wide spectrum of conditions, including neurodegenerative disorders, cardiovascular disease, cancer, metabolic dysfunction, immune dysregulation, and aging. Understanding how mitochondrial form and function intersect with cellular and tissue-level outcomes remains a central challenge in modern biomedical research.
Despite rapid advances, the field faces persistent conceptual and translational challenges. Mitochondrial behavior is highly context-specific, varying across cell types, developmental stages, and disease states, making cross-study comparisons difficult. Establishing causal relationships between morphological changes and functional impairment remains complex, and the relevance of findings from experimental models to human pathology is not always clear. Additionally, integrating structural, functional, and systemic readouts into cohesive biological interpretations continues to be an ongoing challenge.
This Collection aims to present an integrated view of mitochondrial biology in health and disease by bringing together research articles, reviews, and methodological contributions that address mitochondrial structure or function within broader biological and pathological contexts.
By consolidating diverse article contributions across basic, translational, and disease-focused research, this Collection will provide the scientific community with a unified resource to advance understanding of mitochondrial contributions to health and disease and to stimulate interdisciplinary collaboration and innovation.
Transmission Electron Microscopy and FIJI/ImageJ Analysis of Mitochondrial Morphology in Human Skeletal Muscle
Alfonso Carriel1,
Cristobal Munoz1,
Cata Krauss1,
Mauricio Castro-Sepulveda*1
1Laboratorio de Fisiología del Ejercicio y Metabolismo (LABFEM), Escuela de Kinesiología, Facultad de Medicina, Universidad Finis Terrae, Santiago, Chile.
Unbiased, Automated Analysis of Mito–Nuclear Contact Sites
Sahana Mitra1,
Rachael Thomas1,
Tyler Kwok1,
Valentina Perissi*1,
Michael Blower*1
1Boston University, Chobanian & Avedisian School of Medicine, Biochemistry & Cell Biology Department