Commentary 10.1172/JCI125433
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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Elrod, J.
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First published December 3, 2018 - More info
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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