O-36 - Hepatic FMO3 expression and an FMO3-region SNP segregate with atherosclerosis, TMAO, and (inversely) HDL in a mouse F2 cross
Own mouse genetics: host genetic variation controlling TMAO production tracks atherosclerosis, an independent (non-dietary) line supporting a causal role for the TMAO axis.
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Why this is evidence
FMO3 (the TMA→TMAO enzyme) and an FMO3-region SNP co-segregating with lesion area and plasma TMAO is a natural-experiment / Mendelian-randomization-type link between TMAO production and atherosclerosis. Expected under H-15 and H-16; not under H-45, where TMAO is a marker and a TMAO-generating locus should not track disease. Separates the marker pole from the mechanism poles.