ALDH2 regulates a new mechanism for foam cell formation.

On October 31st, the international academic journal The Journal of Clinical Investigation published the research paper "Acethitdehydrogenase 2 Interactions with LDLR and K AMP Foam Foam Cell Cell Formation" by Yu Huiyong of the Shanghai Institute of Life Sciences (Institute of Nutrition and Health) of the Chinese Academy of Sciences.
the study, through cell, animal, and clinical trials, has found that acetaldehyde dehydrogenase 2 (Acetaldehyde dehydrogenase 2, ALDH2) regulates the formation of foam cells and atherosclerosis plaques by interacting with low density lipoprotein receptors (Low Density Lipoprotein Receptor, LDLR) and AMPK.
cardiovascular disease is the world's highest mortality disease, atherosclerosis is the main cause of morbidity and mortality.
in the development of atherosclerosis, macrophages mainly through the ingestion of oxidizing ldl," the formation of foam cells deposited in the endovascular membrane to promote the formation of atherosclerosis plaques.
ALDH2 is an aldehyde dehydrogenase that relies on NAD (P) plus, and about 30-50% of East Asians carry ALDH2 x 2 mutation (rs671), which is significantly reduced in activity of these SNP carriers, characterized by redness after drinking.
in recent years, studies have reported higher rates of cardiovascular events in people with ALDH2rs671-bit mutations, but the molecular mechanisms of ALDH2 and rs671 that affect atherosclerosis are unclear.
Ph.D. student Zhong Shanshan and others, under the guidance of researcher Yu Huiyong, found that the area of atherosclerosis plaquein in LDR2 and LDLR double-knocking mice decreased, and its phenotypes were the opposite of those of alDH2 and ApoE double-knocked mouse phenotypes.
further molecular mechanism studies have found that AMPK phosphorylation activates rs671-bit mutation in macrophages to bind it from the mitochondria to the nucleus of the cell and HDAC3 protein, inhibiting hydrogen ions that regulate lysozyme function and cell autophagy The expression of pump ATP6V0E2 inhibits the hydrolysis of macrophages on oxLDL, causing its build-up in macrophages and promoting the formation of foam cells;
the study found a new mechanism for ALDH2 to regulate the formation of foam cells, explained the increase in cardiovascular disease in people with ALDH2 rs671 dot mutations, and provided new ideas for the treatment of atherosclerosis.
the research was supported by Wu Yuncheng, professor of neurology at the First People's Hospital affiliated with Shanghai Jiaotong University, and Zhang Zhang, a professor at Alberta University in Canada.
the research is supported by the Ministry of Science and Technology, the National Natural Science Foundation of China and the Chinese Academy of Sciences.
Source: Shanghai Institute of Nutrition and Health.