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While the precise mechanism underlying CD38 upregulation in these pathological conditions and disease models are not fully understood, CD38-mediated NAD + consumption leading to NAD + decline and consequent loss of cellular sirtuin activity appears to be a universal mechanism underlying their pathogenesis 24,31
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1,2,3 PAD, most commonly caused by atherosclerotic obstruction of the lower extremity arteries, impairs oxygen and nutrient delivery, resulting in clinical manifestations ranging from intermittent claudication to critical limb-threatening ischemia
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