Electroacupuncture regulates hepatic cholesterol synthesis by HMGCR deubiquitination in rats

Jin, Shu-wen; Han, Yong-li; Pan, Xiao-li; Zhang, Hong-xing

doi:10.1016/j.heliyon.2023.e21005

Cited by 1 publication

(1 citation statement)

References 25 publications

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“…Heida A et al fed mice a carbohydrate-rich diet and then found that HMGCR expression was upregulated, leading to increased hepatic and plasma cholesterol levels [ 95 ]. To further validate this finding, the researchers performed a reverse test and found that inhibiting the enzymatic activity of HMGCR can impair the isoprenylation of adipocyte proteins to prevent the browning of adipocytes, thereby lowering cholesterol level [ 96 , 97 ]. They then conducted a Mendelian randomization study on the human HMGCR gene and discovered that variation in the HMGCR gene coding region, which is connected to the regulation of LDL-C, impacts the patient’s risk for AD.…”

Section: Hmgcr As a Therapeutic Target For Admentioning

confidence: 99%

Mechanisms of 3-Hydroxyl 3-Methylglutaryl CoA Reductase in Alzheimer’s Disease

Zhou,

Wu,

Wang

et al. 2023

IJMS

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Alzheimer’s disease (AD) is the most common neurodegenerative disease worldwide and has a high incidence in the elderly. Unfortunately, there is no effective therapy for AD owing to its complicated pathogenesis. However, the development of lipid-lowering anti-inflammatory drugs has heralded a new era in the treatment of Alzheimer’s disease. Several studies in recent years have shown that lipid metabolic dysregulation and neuroinflammation are associated with the pathogenesis of AD. 3-Hydroxyl 3-methylglutaryl CoA reductase (HMGCR) is a rate-limiting enzyme in cholesterol synthesis that plays a key role in cholesterol metabolism. HMGCR inhibitors, known as statins, have changed from being solely lipid-lowering agents to neuroprotective compounds because of their effects on lipid levels and inflammation. In this review, we first summarize the main regulatory mechanism of HMGCR affecting cholesterol biosynthesis. We also discuss the pathogenesis of AD induced by HMGCR, including disordered lipid metabolism, oxidative stress, inflammation, microglial proliferation, and amyloid-β (Aβ) deposition. Subsequently, we explain the possibility of HMGCR as a potential target for AD treatment. Statins-based AD treatment is an ascent field and currently quite controversial; therefore, we also elaborate on the current application prospects and limitations of statins in AD treatment.

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Section: Hmgcr As a Therapeutic Target For Admentioning

confidence: 99%