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The Rise of Mitochondria in Peripheral Arterial Disease Physiopathology: Experimental and Clinical Data
Mégane Pizzimenti1,2, Marianne Riou1,2, Anne-Laure Charles1
1Unistra, Translational Medicine federation of Strasbourg (FMTS), Faculty of Medicine, Team 3072 «Mitochondria, Oxidative Stress and Muscle Protection», 11 rue Humann, 67000 Strasbourg, France.
Abstract:
Peripheral arterial disease (PAD) is a frequent and serious condition, potentially life-threatening and leading to lower-limb amputation. Its pathophysiology is generally related to ischemia-reperfusion cycles, secondary to reduction or interruption of the arterial blood flow followed by reperfusion episodes that are necessary but also-per se-deleterious. Skeletal muscles alterations significantly participate in PAD injuries, and interestingly, muscle mitochondrial dysfunctions have been demonstrated to be key events and to have a prognosis value. Decreased oxidative capacity due to mitochondrial respiratory chain impairment is associated with increased release of reactive oxygen species and reduction of calcium retention capacity leading thus to enhanced apoptosis. Therefore, targeting mitochondria might be a promising therapeutic approach in PAD.
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