2015年9月11日 · It is a mitochondrial enzyme that catalyzes the first reaction of ketogenesis, a metabolic pathway that provides lipid-derived energy for various organs during times of carbohydrate deprivation, such as fasting. Mutations in this gene are associated with HMG-CoA synthase deficiency.

2017年7月4日 · Of these 10 genes, the 3-Hydroxy-3-Methylglutaryl-CoA Synthase 2 (HMGCS2) was the highest upregulated gene in T1D heart. IPA analysis showed that HMGCS2 was center to many biological...

2023年9月5日 · 3-Hydroxymethylglutaryl-CoA synthase 2 (HMGCS2) is the rate-limiting enzyme for ketone body synthesis, and most current studies focus on mitochondrial maturation and metabolic...

HMGCS2 serves as a potential biomarker for inhibition of renal clear cell carcinoma growth. LONP1 targets HMGCS2 to protect mitochondrial function and attenuate chronic kidney disease. Hmgcs2-mediated ketogenesis modulates high-fat diet-induced hepatosteatosis.

Here we aimed to determine the impact of Hmgcs2-mediated ketogenesis and its modulations on the development and treatment of fatty liver disease.

2021年7月26日 · Mitochondrial 3-hydroxy-3-methylglutaryl CoA synthase (HMGCS2; EC 2.3.3.10) mediates the first reaction of ketogenesis, a metabolic pathway that provides lipid-derived energy for brain, heart, kidney, and other organs during times of carbohydrate deprivation such as fasting (Robinson and Williamson, 1980).

2025年1月4日 · Clinical resource with information about HMGCS2, 3-hydroxy-3-methylglutaryl-CoA synthase deficiency, and available tests. There are links to practice guidelines and authoritative resources like GeneReviews, PubMed, MedlinePlus, PharmGKB and clinicaltrials.gov.

2019年9月19日 · Mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase 2 (HMGCS2), a rate-limiting ketogenic enzyme in the synthesis of ketone body β-hydroxybutyrate (βHB), contributes to the regulation of intestinal cell differentiation.

Hepatocyte-specific HMGCS2 knockout (LKO) mice were generated and used to compare the difference in liver metabolic response to fasting between wild-type (WT) and LKO mice. Our findings demonstrate that HMGCS2 is essential in enhanced hepatic ketogenesis during fasting.

In our investigation of the molecular mechanisms of HMGCS2 in HCC, we showed that knockdown of HMGCS2 decreased ketone production, which promoted cell proliferation, cell migration, and xenograft tumorigenesis by enhancing c-Myc/cyclinD1 and EMT signaling and by suppressing the caspase-dependent apoptosis pathway.