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Upregulation of CD38 in patients with SSc, resulting from its induction by cytokines such as TGF-, IL-6 and senescent cell-derived SASP enriched in the fibrotic tissue microenvironment, will promote NAD + consumption and decline, which in turn impairs the function of sirtuins and other NAD + -dependent cellular enzymes

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Proteomic analysis also revealed specific deficits in the mitochondrial ATP synthase (Atp5a1) within complex V and in the ATP/ADP translocase (Slc25a4) (304)

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