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The source of WS is the Werner (WRN) DNA helicase gene, which regulates the transcription of the essential NAD+ biosynthetic enzyme Nicotinamide Nucleotide Adenylyltransferase 1 (24,25). NAD+ depletion through disruption of mitochondrial homeostasis is a substantial contributor to the metabolic dysfunction in WS, according to a 2019 study (25)

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As Nrf2 target genes, HO-1 and NQO1 have been proven to protect cells and inhibit ferroptosis upon Nrf2 activation 63,64

This determines the strongly pro-inflammatory characteristics of this RCD with poorly controlled inflammatory response [128]