Potential of Polyphenols to Restore SIRT1 and NAD+ Metabolism in Renal Disease

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Oryginal text

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119-125

The de novo NAD+ biosynthetic path-way is particularly relevant in the kidney since this organ expresses all NAD+ biosynthetic enzymes, such as indoleamine 2,3-dioxygenase (IDO), quinolinate phosphoribosyltransferase (QPRT), and α-amino-β-carboxymuconate-ε-semialdehyde decarboxylase (ACMSD). Notably, ACMSD forms α-aminomuconate-ε-semialdehyde (AMS), which can be oxidized to CO2 and H2O, inhibiting NAD+ synthesis and reducing NAD+ levels. Genetic and pharmacological inhibition of ACMSD increases NAD+ levels, improving mitochondrial and kidney function

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127 and other lines

ACSMD

Is it the same as ACMSD?

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533-535

Glomerular damage also causes endothelial dysfunction and tubular injury, leading to cell death, endothelial-/epithelial-to- mesenchymal transitions, cell infiltration, tubule degeneration, and interstitial fibrosis mediated through different mechanisms

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545-547

In glomerular visceral epithelial cells or podocytes, which are highly specialized cells in the kidney glomerulus that are essential for preventing plasma proteins from entering 546 the urinary ultrafiltrate and are key participants in the formation of the glomerular filtration barrier

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Figure 4

Please show the resveratrol grip point

3.1.1.1.4

.Whole chapter

Paucity of arguments describing the role of resveratrol.

861-863

Nevertheless, a recent study [277] showed that renal fibrosis was inhibited by treatment of UUO mice with the SIRT1/2 inhibitor sirtinol or SIRT1 inhibitor EX527

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