{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,10]],"date-time":"2026-11-10T17:33:28Z","timestamp":1794332008043,"version":"4.9.0"},"reference-count":88,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"680","content-domain":{"domain":["www.science.org"],"crossmark-restriction":true},"short-container-title":["Sci. Transl. Med."],"published-print":{"date-parts":[[2023,1,25]]},"abstract":"<jats:p>The common aldehyde dehydrogenase 2 (<jats:italic>ALDH2<\/jats:italic>) alcohol flushing variant known as<jats:italic>ALDH2*2<\/jats:italic>affects \u223c8% of the world\u2019s population. Even in heterozygous carriers, this missense variant leads to a severe loss of ALDH2 enzymatic activity and has been linked to an increased risk of coronary artery disease (CAD). Endothelial cell (EC) dysfunction plays a determining role in all stages of CAD pathogenesis, including early-onset CAD. However, the contribution of<jats:italic>ALDH2*2<\/jats:italic>to EC dysfunction and its relation to CAD are not fully understood. In a large genome-wide association study (GWAS) from Biobank Japan,<jats:italic>ALDH2*2<\/jats:italic>was found to be one of the strongest single-nucleotide polymorphisms associated with CAD. Clinical assessment of endothelial function showed that human participants carrying<jats:italic>ALDH2*2<\/jats:italic>exhibited impaired vasodilation after light alcohol drinking. Using human induced pluripotent stem cell\u2013derived ECs (iPSC-ECs) and CRISPR-Cas9\u2013corrected<jats:italic>ALDH2*2<\/jats:italic>iPSC-ECs, we modeled<jats:italic>ALDH2*2<\/jats:italic>-induced EC dysfunction in vitro, demonstrating an increase in oxidative stress and inflammatory markers and a decrease in nitric oxide (NO) production and tube formation capacity, which was further exacerbated by ethanol exposure. We subsequently found that sodium-glucose cotransporter 2 inhibitors (SGLT2i) such as empagliflozin mitigated<jats:italic>ALDH2*2<\/jats:italic>-associated EC dysfunction. Studies in<jats:italic>ALDH2*2<\/jats:italic>knock-in mice further demonstrated that empagliflozin attenuated<jats:italic>ALDH2*2<\/jats:italic>-mediated vascular dysfunction in vivo. Mechanistically, empagliflozin inhibited Na<jats:sup>+<\/jats:sup>\/H<jats:sup>+<\/jats:sup>-exchanger 1 (NHE-1) and activated AKT kinase and endothelial NO synthase (eNOS) pathways to ameliorate<jats:italic>ALDH2*2<\/jats:italic>-induced EC dysfunction. Together, our results suggest that<jats:italic>ALDH2*2<\/jats:italic>induces EC dysfunction and that SGLT2i may potentially be used as a preventative measure against CAD for<jats:italic>ALDH2*2<\/jats:italic>carriers.<\/jats:p>","DOI":"10.1126\/scitranslmed.abp9952","type":"journal-article","created":{"date-parts":[[2023,1,25]],"date-time":"2023-01-25T18:58:12Z","timestamp":1674673092000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":53,"title":["SGLT2 inhibitor ameliorates endothelial dysfunction associated with the common<i>ALDH2<\/i>alcohol flushing variant"],"prefix":"10.1126","volume":"15","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8884-7358","authenticated-orcid":true,"given":"Hongchao","family":"Guo","sequence":"first","affiliation":[{"name":"Stanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA."},{"name":"Institute for Stem Cell Biology and Regenerative Medicine, 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