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Redox Biology published online the latest research results of Acetaldehyde Dehydrogenase 2 Regulates HMG-CoA Reductase Stability and Cholesterol Synthesis in the Liver by Yin Huiyong's group from Shanghai Institute of Nutrition and Health, Chinese Academy of Sciences.
The study revealed that Acetaldehyde Dehydrogenase 2 (ALDH2) regulates a key rate-resolving enzyme in the de novo synthesis of cholesterol in the liver, 3-hydroxy-3-methylglutaryl-CoA reductase (3 -hydroxy-3-methyl glutaryl coenzyme A reductase (HMGCR) protein stability to affect the new mechanism of cholesterol metabolism.
The study revealed that Acetaldehyde Dehydrogenase 2 (ALDH2) regulates a key rate-resolving enzyme in the de novo synthesis of cholesterol in the liver, 3-hydroxy-3-methylglutaryl-CoA reductase (3 -hydroxy-3-methyl glutaryl coenzyme A reductase (HMGCR) protein stability to affect the new mechanism of cholesterol metabolism.
The incidence and mortality of cardiovascular diseases are relatively high, and atherosclerosis is one of the main reasons for the occurrence and development of cardiovascular diseases.
High serum cholesterol level is an independent risk factor for cardiovascular disease.
Lowering cholesterol is the main means to prevent and treat atherosclerosis and cardiovascular disease.
Nowadays, statins, the first-line cholesterol-lowering drug in clinical practice, target HMGCR to inhibit cholesterol synthesis.
High serum cholesterol level is an independent risk factor for cardiovascular disease.
Lowering cholesterol is the main means to prevent and treat atherosclerosis and cardiovascular disease.
Nowadays, statins, the first-line cholesterol-lowering drug in clinical practice, target HMGCR to inhibit cholesterol synthesis.
Aldehyde dehydrogenase 2 (ALDH2) is mainly responsible for catalyzing the oxidation of acetaldehyde produced by drinking to acetic acid, and metabolizing active aldehydes produced by oxidative stress lipid peroxidation.
In the process of atherosclerosis, lipid peroxidation and inflammation are two important risk factors.
There is a nucleotide polymorphism (SNP, rs671) in the human body.
People who carry this mutation may blush after drinking alcohol due to decreased ALDH2 enzyme activity.
The mutation affects 8% of the global population, and 30-50% of the Asian population carry the mutation.
Data from population studies show that in addition to drinking facial infrared, the risk of cardiovascular disease in these populations is also significantly increased, and the relevant molecular mechanisms need to be further clarified.
Preliminary studies in the laboratory found that ALHD2 interacts with low-density lipoprotein receptors LDLR and AMPK to affect the formation of foamy macrophages (J Clin Invest, 2019), and for the first time clarified that an ALDH2 mutation increases the risk of atherosclerosis independent of Molecular mechanisms other than drinking.
In addition, previous population data also showed that ALDH2 mutations are related to cholesterol metabolism, but the molecular mechanism is unknown.
In the process of atherosclerosis, lipid peroxidation and inflammation are two important risk factors.
There is a nucleotide polymorphism (SNP, rs671) in the human body.
People who carry this mutation may blush after drinking alcohol due to decreased ALDH2 enzyme activity.
The mutation affects 8% of the global population, and 30-50% of the Asian population carry the mutation.
Data from population studies show that in addition to drinking facial infrared, the risk of cardiovascular disease in these populations is also significantly increased, and the relevant molecular mechanisms need to be further clarified.
Preliminary studies in the laboratory found that ALHD2 interacts with low-density lipoprotein receptors LDLR and AMPK to affect the formation of foamy macrophages (J Clin Invest, 2019), and for the first time clarified that an ALDH2 mutation increases the risk of atherosclerosis independent of Molecular mechanisms other than drinking.
In addition, previous population data also showed that ALDH2 mutations are related to cholesterol metabolism, but the molecular mechanism is unknown.
In the study, researchers observed in ALDH2 knockout and rs671 knock-in mice that even feeding ordinary foods caused an increase in total cholesterol and low-density lipoprotein levels in the liver and serum.
Using metabolomics and metabolic flow analysis, it was found that cholesterol synthesis in ALDH2 knockout mice was increased; the increase in cholesterol levels in mice could be inhibited by statins, suggesting that ALDH2 may be involved in the regulation of cholesterol synthase HMGCR.
In cell experiments, studies have found that ALDH2 directly affects the ubiquitination and degradation of HMGCR: ALDH2 promotes the interaction between HMGCR and Insig1/SCAP/gp78 and inhibits cholesterol synthesis.
This effect is significantly weakened in ALDH2 mutants.
Further mechanism studies have shown that when cholesterol is elevated, mitochondrial ALDH2 is transferred to the endoplasmic reticulum (Mitochondria-Associated membrane with ER, MAM) through the mitochondrial-associated membrane with ER (MAM), which promotes the ubiquitination and degradation of HMGCR.
In the ALDH2 knockout or rs671 knock-in model, the protein stability of HMGCR increases to promote cholesterol synthesis (as shown in the figure).
The study discovered a new mechanism for the regulation of cholesterol metabolism, and suggested that the increased risk of cardiovascular disease in ALDH2 mutant populations may be related to the disorder of cholesterol metabolism; the clinical cholesterol-lowering drug statins can effectively inhibit the increase in cholesterol levels.
(bioon.
com" target="_blank">Bioon.
com)
Using metabolomics and metabolic flow analysis, it was found that cholesterol synthesis in ALDH2 knockout mice was increased; the increase in cholesterol levels in mice could be inhibited by statins, suggesting that ALDH2 may be involved in the regulation of cholesterol synthase HMGCR.
In cell experiments, studies have found that ALDH2 directly affects the ubiquitination and degradation of HMGCR: ALDH2 promotes the interaction between HMGCR and Insig1/SCAP/gp78 and inhibits cholesterol synthesis.
This effect is significantly weakened in ALDH2 mutants.
Further mechanism studies have shown that when cholesterol is elevated, mitochondrial ALDH2 is transferred to the endoplasmic reticulum (Mitochondria-Associated membrane with ER, MAM) through the mitochondrial-associated membrane with ER (MAM), which promotes the ubiquitination and degradation of HMGCR.
In the ALDH2 knockout or rs671 knock-in model, the protein stability of HMGCR increases to promote cholesterol synthesis (as shown in the figure).
The study discovered a new mechanism for the regulation of cholesterol metabolism, and suggested that the increased risk of cardiovascular disease in ALDH2 mutant populations may be related to the disorder of cholesterol metabolism; the clinical cholesterol-lowering drug statins can effectively inhibit the increase in cholesterol levels.
(bioon.
com" target="_blank">Bioon.
com)
Redox Biology published online the latest research results of Acetaldehyde Dehydrogenase 2 Regulates HMG-CoA Reductase Stability and Cholesterol Synthesis in the Liver by Yin Huiyong's group from Shanghai Institute of Nutrition and Health, Chinese Academy of Sciences.
The study revealed that Acetaldehyde Dehydrogenase 2 (ALDH2) regulates a key rate-resolving enzyme in the de novo synthesis of cholesterol in the liver, 3-hydroxy-3-methylglutaryl-CoA reductase (3 -hydroxy-3-methyl glutaryl coenzyme A reductase (HMGCR) protein stability to affect the new mechanism of cholesterol metabolism.
The study revealed that Acetaldehyde Dehydrogenase 2 (ALDH2) regulates a key rate-resolving enzyme in the de novo synthesis of cholesterol in the liver, 3-hydroxy-3-methylglutaryl-CoA reductase (3 -hydroxy-3-methyl glutaryl coenzyme A reductase (HMGCR) protein stability to affect the new mechanism of cholesterol metabolism.
The incidence and mortality of cardiovascular diseases are relatively high, and atherosclerosis is one of the main reasons for the occurrence and development of cardiovascular diseases.
High serum cholesterol level is an independent risk factor for cardiovascular disease.
Lowering cholesterol is the main means to prevent and treat atherosclerosis and cardiovascular disease.
Nowadays, statins, the first-line cholesterol-lowering drug in clinical practice, target HMGCR to inhibit cholesterol synthesis.
High serum cholesterol level is an independent risk factor for cardiovascular disease.
Lowering cholesterol is the main means to prevent and treat atherosclerosis and cardiovascular disease.
Nowadays, statins, the first-line cholesterol-lowering drug in clinical practice, target HMGCR to inhibit cholesterol synthesis.
Aldehyde dehydrogenase 2 (ALDH2) is mainly responsible for catalyzing the oxidation of acetaldehyde produced by drinking to acetic acid, and metabolizing active aldehydes produced by oxidative stress lipid peroxidation.
In the process of atherosclerosis, lipid peroxidation and inflammation are two important risk factors.
There is a nucleotide polymorphism (SNP, rs671) in the human body.
People who carry this mutation may blush after drinking alcohol due to decreased ALDH2 enzyme activity.
The mutation affects 8% of the global population, and 30-50% of the Asian population carry the mutation.
Data from population studies show that in addition to drinking facial infrared, the risk of cardiovascular disease in these populations is also significantly increased, and the relevant molecular mechanisms need to be further clarified.
Preliminary studies in the laboratory found that ALHD2 interacts with low-density lipoprotein receptors LDLR and AMPK to affect the formation of foamy macrophages (J Clin Invest, 2019), and for the first time clarified that an ALDH2 mutation increases the risk of atherosclerosis independent of Molecular mechanisms other than drinking.
In addition, previous population data also showed that ALDH2 mutations are related to cholesterol metabolism, but the molecular mechanism is unknown.
In the process of atherosclerosis, lipid peroxidation and inflammation are two important risk factors.
There is a nucleotide polymorphism (SNP, rs671) in the human body.
People who carry this mutation may blush after drinking alcohol due to decreased ALDH2 enzyme activity.
The mutation affects 8% of the global population, and 30-50% of the Asian population carry the mutation.
Data from population studies show that in addition to drinking facial infrared, the risk of cardiovascular disease in these populations is also significantly increased, and the relevant molecular mechanisms need to be further clarified.
Preliminary studies in the laboratory found that ALHD2 interacts with low-density lipoprotein receptors LDLR and AMPK to affect the formation of foamy macrophages (J Clin Invest, 2019), and for the first time clarified that an ALDH2 mutation increases the risk of atherosclerosis independent of Molecular mechanisms other than drinking.
In addition, previous population data also showed that ALDH2 mutations are related to cholesterol metabolism, but the molecular mechanism is unknown.
In the study, researchers observed in ALDH2 knockout and rs671 knock-in mice that even feeding ordinary foods caused an increase in total cholesterol and low-density lipoprotein levels in the liver and serum.
Using metabolomics and metabolic flow analysis, it was found that cholesterol synthesis in ALDH2 knockout mice was increased; the increase in cholesterol levels in mice could be inhibited by statins, suggesting that ALDH2 may be involved in the regulation of cholesterol synthase HMGCR.
In cell experiments, studies have found that ALDH2 directly affects the ubiquitination and degradation of HMGCR: ALDH2 promotes the interaction between HMGCR and Insig1/SCAP/gp78 and inhibits cholesterol synthesis.
This effect is significantly weakened in ALDH2 mutants.
Further mechanism studies have shown that when cholesterol is elevated, mitochondrial ALDH2 is transferred to the endoplasmic reticulum (Mitochondria-Associated membrane with ER, MAM) through the mitochondrial-associated membrane with ER (MAM), which promotes the ubiquitination and degradation of HMGCR.
In the ALDH2 knockout or rs671 knock-in model, the protein stability of HMGCR increases to promote cholesterol synthesis (as shown in the figure).
The study discovered a new mechanism for the regulation of cholesterol metabolism, and suggested that the increased risk of cardiovascular disease in ALDH2 mutant populations may be related to the disorder of cholesterol metabolism; the clinical cholesterol-lowering drug statins can effectively inhibit the increase in cholesterol levels.
(bioon.
com" target="_blank">Bioon.
com)
bioon. Using metabolomics and metabolic flow analysis, it was found that cholesterol synthesis in ALDH2 knockout mice was increased; the increase in cholesterol levels in mice could be inhibited by statins, suggesting that ALDH2 may be involved in the regulation of cholesterol synthase HMGCR.
In cell experiments, studies have found that ALDH2 directly affects the ubiquitination and degradation of HMGCR: ALDH2 promotes the interaction between HMGCR and Insig1/SCAP/gp78 and inhibits cholesterol synthesis.
This effect is significantly weakened in ALDH2 mutants.
Further mechanism studies have shown that when cholesterol is elevated, mitochondrial ALDH2 is transferred to the endoplasmic reticulum (Mitochondria-Associated membrane with ER, MAM) through the mitochondrial-associated membrane with ER (MAM), which promotes the ubiquitination and degradation of HMGCR.
In the ALDH2 knockout or rs671 knock-in model, the protein stability of HMGCR increases to promote cholesterol synthesis (as shown in the figure).
The study discovered a new mechanism for the regulation of cholesterol metabolism, and suggested that the increased risk of cardiovascular disease in ALDH2 mutant populations may be related to the disorder of cholesterol metabolism; the clinical cholesterol-lowering drug statins can effectively inhibit the increase in cholesterol levels.
(bioon.
com" target="_blank">Bioon.
com)
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