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Abstract We have previously proposed that the heterogeneous collapse of mitochondrial inner membrane potential ( m ) during ischemia and reperfusion contributes to arrhythmogenesis through the formation of metabolic sinks in the myocardium, wherein clusters of myocytes with uncoupled mitochondria and high K ATP current levels alter electrical propagation to promote reentry

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NAD+ decline is now understood as a driver of the mitochondrial dysfunction that underlies much of the physical and cognitive decline associated with aging

Studies indicate that BPC-157 has been evaluated in models involving muscle tissue, tendons, ligaments, gastrointestinal mucosa and other structures exposed to mechanical or inflammatory damage