Xu G, Zhao J, Liu H, Wang J, Lu W
Rudnicka L, Kaczorowska A
A patient with gout has been shown in a broad range of studies to be at higher risk of coronary disease , and should have an evaluation appropriate to coronary risk (for example, lab testing for cholesterol and triglyceride level).3 It is important that damage to bone from gout be diagnosed, since documented damage is a clear indication for long-term therapy (see below)
Beyond FSP1 there are therapeutic opportunities across the CoQ 10 oxidoreductase network While FSP1 currently has the strongest targetability signal, other CoQ 10 oxidoreductases may be therapeutically leveraged in defined genetic, metabolic or tissue contexts: (1) DHODH axis (mitochondrial defense in select contexts): DHODH connects pyrimidine synthesis to mitochondrial CoQ reduction, and in some settings, DHODH inhibition has been proposed to heighten ferroptosis sensitivity, especially in GPX4-low states