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S1P which is abundant in blood constituents, principally in erythrocytes and platelets, has an important role in the proliferation of endometriotic cells [44]

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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