Mitochondrial Dysfunction in Disease 2.0

Dear Colleagues,

Mitochondria are the powerhouse of the cell, producing chemical energy in the form of adenosine triphosphate (ATP) in a process termed oxidative phosphorylation. The proper function of mitochondria depends on their biogenesis, morphology, and bioenergetic capacity. In addition to their role in cellular respiration and energy production, they have critical functions in intracellular calcium homeostasis, cell growth and death, regulation of oxidative radicals, and production of biosynthetic molecules. The morphology, number, and function of mitochondria are a characteristic unique to each tissue to meet the energy needs of the organ. Indeed, mitochondria are not mere bystanders constrained by the cells they are contained within but highly dynamic and responsive organelles participating in intracellular signaling and highly regulated in both health and disease. As such, mitochondria have gained attention as a therapeutic target with great promise. Dysfunction of mitochondria is recognized in metabolic diseases, ischemic-tissue injury, cancer, neurodegenerative disease, and chronic kidney disease, just to name a few. This Special Issue highlights the most recent research on how mitochondrial dysfunction contributes to disease. We cordially invite authors to contribute original research and review articles focusing on the role of mitochondria in disease and its progression. Novel mitochondrial-based therapies with translational potential, strategies targeting mitochondrial biogenesis, clearance, and signaling would be of interest. Genetic and mitochondrial replacement therapy approaches to mitochondrial dysfunction would be of interest with challenges unique to the mitochondria. We hope our Special Edition will reflect current and novel insights into the role of mitochondria in disease.

Dr. Daniel L Galvan
Guest Editor

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

• oxidative phosphorylation
• mitophagy
• mitochondrial disease
• diabetes
• mitochondrial transport
• electron transport chain
• amino acid metabolism
• lipid metabolism
• cardiolipin
• mitochondrial replacement

• Mitochondrial Dysfunction in Disease in Biomedicines (11 articles)