Not just correlative: a new pathway defines how an ALDH2 SNP contributes to atherosclerosis
Andrew A. Gibb and John W. Elrod
Center for Translational Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, Pennsylvania, USA.
Address correspondence to: John W. Elrod, Center for Translational Medicine, Lewis Katz School of Medicine at Temple University, 3500 N. Broad Street, MERB 949, Philadelphia, Pennsylvania 19140, USA. Phone: 215.707.5480; Email: elrod@temple.edu.
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Center for Translational Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, Pennsylvania, USA.
Address correspondence to: John W. Elrod, Center for Translational Medicine, Lewis Katz School of Medicine at Temple University, 3500 N. Broad Street, MERB 949, Philadelphia, Pennsylvania 19140, USA. Phone: 215.707.5480; Email: elrod@temple.edu.
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First published December 3, 2018 - More info
J Clin Invest. 2019;129(1):63–65. https://doi.org/10.1172/JCI125433.
Copyright © 2019, American Society for Clinical Investigation
Individuals with the rs671 SNP in the gene encoding aldehyde dehydrogenase 2 (ALDH2) are at increased risk of cardiovascular disease (CVD); however, it has been unclear if this mutation contributes to CVD development. In this issue of the JCI, Zhong et al. perform an elegant set of experiments that reveal a pathway wherein the ALDH2 rs671 mutant is phosphorylated by AMPK and translocates to the nucleus where it represses the transcription of a lysosomal H+ pump subunit that is critical for lipid degradation and foam cell formation, as occurs in atherosclerosis. The discovery of this pathway may explain how subjects harboring ALDH2 rs671 are at a greater risk for numerous other disease states and thereby provide new targets for therapeutic intervention.
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