Mitochondria, powerhouse of the cell, malfunctioning causes serious consequences that might be responsible for a wide range of disease pathologies including cancer, diabetes, neurodegenerative diseases, and so on. Altered mitochondrial morphology, excessive generation of reactive oxygen species, and disturbances in oxidative phosphorylation, resulting in a decline in adenosine triphosphate production. Mitochondria are important for the metabolism of energy, regulation of apoptosis, and signalling of cells. In malignant cells, mitochondria differ structurally and functionally from those in normal cells and actively participate in metabolic reprogramming. overproduction of reactive oxygen species (ROS), which encourages the development of cancer by causing genomic instability, altering gene expression, and participating in signalling pathways. Mutations in mitochondrial and nuclear DNA induced by oxidative damage that impairs the oxidative phosphorylation mechanism can lead to further production of mitochondrial ROS, completing the “vicious cycle” between mitochondria, ROS, genomic instability, and cancer development. Impaired signalling pathways disturb the normal cell cycle, which then leads to the development of a plethora of pathological conditions including neurodegenerative diseases and cancer. In the last decade, tremendous progress has been made in understanding mitochondrial structure, function, and their physiology in metabolic syndromes such as diabetes, obesity, stroke and hypertension, and heart disease. Further, progress has also been made in developing therapeutic strategies, including lifestyle interventions (healthy diet and regular exercise), pharmacological strategies and mitochondria-targeted approaches. These strategies were mainly focused to reduce mitochondrial dysfunction and oxidative stress and to maintain mitochondrial quality in metabolic syndromes.
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