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- W3149706243 endingPage "325" @default.
- W3149706243 startingPage "325" @default.
- W3149706243 abstract "Human diseases range from gene-associated to gene-non-associated disorders, including age-related diseases, neurodegenerative, neuromuscular, cardiovascular, diabetic diseases, neurocognitive disorders and cancer. Mitochondria participate to the cascades of pathogenic events leading to the onset and progression of these diseases independently of their association to mutations of genes encoding mitochondrial protein. Under physiological conditions, the mitochondrial ATP synthase provides the most energy of the cell via the oxidative phosphorylation. Alterations of oxidative phosphorylation mainly affect the tissues characterized by a high-energy metabolism, such as nervous, cardiac and skeletal muscle tissues. In this review, we focus on human diseases caused by altered expressions of ATP synthase genes of both mitochondrial and nuclear origin. Moreover, we describe the contribution of ATP synthase to the pathophysiological mechanisms of other human diseases such as cardiovascular, neurodegenerative diseases or neurocognitive disorders." @default.
- W3149706243 created "2021-04-13" @default.
- W3149706243 creator A5003543778 @default.
- W3149706243 creator A5031996070 @default.
- W3149706243 creator A5057433492 @default.
- W3149706243 creator A5064932458 @default.
- W3149706243 date "2021-04-08" @default.
- W3149706243 modified "2023-10-16" @default.
- W3149706243 title "The ATP Synthase Deficiency in Human Diseases" @default.
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