Impaired Mitochondrial Bioenergetics under Pathological Conditions

Dear colleagues,

Mitochondria, being involved in multiple metabolic functions to power life, also emerge as crucial cell components in a variety of diseases. A diffused reaction to pathology is a mitochondrial dysfunction that causes energy depletion and commits the cell to die. The mitochondrial involvement in diseases is highlighted by distinct changes in mitochondrial homeostasis. The altered metabolic pathways impair oxidative phosphorylation and the AMP/ATP ratio. Mitochondria produce ROS, resulting from the disassembly of respiratory supercomplexes and electron transfer chain disruption. The progressive dysregulation of mitochondrial homeostasis promotes Ca²⁺ overload in the matrix and ROS accumulation, leading to the so-called ROS-induced ROS release. When ROS levels became toxic, they damage mitochondrial and nuclear DNA and the cell cycle arrests. Moreover, elevated Ca²⁺ levels in the matrix and oxidative stress induce the mitochondrial permeability transition pore formation, a high-conductance channel that dissipates the mitochondrial protonomotive force resulting in mitochondrial swelling, membrane rupture, bioenergetic failure, and ultimately cell death. Lastly, the parallelism of mitochondrial dysregulation and morphological changes in mitochondria highlights the tight connection between mitochondrial membrane dynamics and pathologies.

Finally, studies on the impaired mitochondrial bioenergetics in pathology could provide molecular tools to counteract diseases associated with mitochondrial dysfunctions.

Prof. Dr. Giorgio Lenaz
Dr. Salvatore Nesci
Guest Editors

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