Mechanisms of Acetaldehyde-Induced Organ Injury via Impairment of Vascular Endothelial Cells

Ming-Zhang Xie,1,2,* Jia-Qi Dong,3,* Chun Guo,1,4 Shi-Qi Ge,3 Rui-Xiang Sun,5 Fei Lin6 1Department of Genetics, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, Henan, 453000, People’s Republic of China; 2Department of Pharmacy, Luohe Medical College, Luohe, Henan, 462002, People’s Republic of China; 3Department of Cardiovascular, The Fourth Clinical College of Xinxiang Medical University, Xinxiang, Henan, 453001, People’s Republic of China; 4Department of Human Anatomy, School of Basic Medical Sciences, Youjiang Medical University for Nationalities, Baise, Guangxi, 533000, People’s Republic of China; 5Department of Cardiovascular, The Third Clinical College of Xinxiang Medical University, Xinxiang, Henan, 453001, People’s Republic of China; 6Department of Cardiovascular, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, Henan, 453000, People’s Republic of China*These authors contributed equally to this workCorrespondence: Fei Lin, Department of Cardiovascular, First Affiliated Hospital of Xinxiang Medical University, Xinxiang, Henan, 453000, People’s Republic of China, Tel +86 13663868285, Email [email protected]: Acetaldehyde, a metabolite of alcohol, accumulates in the body through excessive alcohol consumption. This accumulation triggers a range of vascular endothelial cell damage, including changes of signaling pathways, and ultimately results in organ and tissue damage. In this review, we highlight the role of acetaldehyde in vascular endothelial cell damage, including DNA damage, oxidative stress, and changes in signaling pathways. Particularly concerning the role of the NEIL3 pathway in DNA repair, the NEIL3 pathway is prioritized over the Fanconi anemia pathway, which may result in genomic rearrangements and the cleavage of the crosslink. Insulin, and estrogen receptors α damage induced by acetaldehyde. Notably, we describe the mechanisms by which long-term acetaldehyde exposure causes DNA damage, oxidative stress, imbalance in Ca2+ homeostasis, inflammatory response, and signaling pathway changes. We provide novel insights into the intervention of acetaldehyde exposure-mediated vascular endothelial cell disorders. Keywords: acetaldehyde, laboratory targets, toxicity, vascular injury