ArticleInternational journal of molecular sciences2023
Acute ACAT1/SOAT1 Blockade Increases MAM Cholesterol and Strengthens ER-Mitochondria Connectivity.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 31 citations in OpenAlex.
- An integrated multiomic single-vesicle atlas delineates graft exosome heterogeneity in chronic lung allograft dysfunction.Signal transduction and targeted therapy · 2026Article
- Macrophage ACAT1 Aggravates Alcohol-Associated Liver Disease by Inducing Mitochondrial Damage and NLRP3 Activation.Journal of gastroenterology and hepatology · 2026Article
- Organelle Crosstalk in Renal Cells: Insights from Cell Biology and Implications for AKI-to-CKD Transition.International journal of molecular sciences · 2026Review
- Article
- Impaired lipoprotein secretion by APOE4 leads to lysosomal and mitochondrial dysfunction in human microglia.bioRxiv : the preprint server for biology · 2026Article
- Adrenocortical Mitochondria-Associated Membranes: Isolation, Characterization, and Lipidoproteomic Response to Mitotane.Journal of the Endocrine Society · 2026Article
- The role of mitochondrial-associated endoplasmic reticulum membranes (MAMs) in diabetic microvascular complications: a review.Cell death & disease · 2025Review
- N4-acetylcytidine-mediated SOAT1 upregulation aggravates heart failure by inducing NCOA4-dependent ferroautophagy and ferroptosis in cardiomyocytes.Cellular and molecular life sciences : CMLS · 2025Article
- The complex web of membrane contact sites in brain aging and neurodegeneration.Cellular and molecular life sciences : CMLS · 2025Review
- Review
- Integrative eQTL and Mendelian randomization analysis reveals key genetic markers in mesothelioma.Respiratory research · 2025Article
- CPT1A-mediated MFF succinylation promotes stemness maintenance in ovarian cancer stem cells.Communications biology · 2025Article
- Remodeling of Mitochondria-Endoplasmic Reticulum Contact Sites Accompanies LUHMES Differentiation.Biomolecules · 2025Article
- Mitochondrial and ER stress crosstalk in TBI: mechanistic insights and therapeutic opportunities.Frontiers in cellular neuroscience · 2025Review
- Inhibiting the Cholesterol Storage Enzyme ACAT1/SOAT1 in Aging Apolipoprotein E4 Mice Alters Their Brains' Inflammatory Profiles.International journal of molecular sciences · 2024Article
- The contribution of mitochondria-associated ER membranes to cholesterol homeostasis.bioRxiv : the preprint server for biology · 2024Article
- Inhibiting the Cholesterol Storage Enzyme ACAT1/SOAT1 in Myelin Debris-Treated Microglial Cell Lines Activates the Gene Expression of Cholesterol Efflux Transporter ABCA1.Biomolecules · 2024Article
- Unveiling differential gene co-expression networks and its effects on levodopa-induced dyskinesia.iScience · 2024Article
- Inhibition of sterol O-acyltransferase 1 blocks Zika virus infection in cell lines and cerebral organoids.Communications biology · 2024Article
- Characterization of Stealth Liposome-Based Nanoparticles Encapsulating the ACAT1/SOAT1 Inhibitor F26: Efficacy and Toxicity Studies In Vitro and in Wild-Type Mice.International journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Cholesterol is a key component of all mammalian cell membranes. Disruptions in cholesterol metabolism have been observed in the context of various diseases, including neurodegenerative disorders such as Alzheimer's disease (AD). The genetic and pharmacological blockade of acyl-CoA:cholesterol acyltransferase 1/sterol O-acyltransferase 1 (ACAT1/SOAT1), a cholesterol storage enzyme found on the endoplasmic reticulum (ER) and enriched at the mitochondria-associated ER membrane (MAM), has been shown to reduce amyloid pathology and rescue cognitive deficits in mouse models of AD. Additionally, blocking ACAT1/SOAT1 activity stimulates autophagy and lysosomal biogenesis; however, the exact molecular connection between the ACAT1/SOAT1 blockade and these observed benefits remain unknown. Here, using biochemical fractionation techniques, we observe cholesterol accumulation at the MAM which leads to ACAT1/SOAT1 enrichment in this domain. MAM proteomics data suggests that ACAT1/SOAT1 inhibition strengthens the ER-mitochondria connection. Confocal and electron microscopy confirms that ACAT1/SOAT1 inhibition increases the number of ER-mitochondria contact sites and strengthens this connection by shortening the distance between these two organelles. This work demonstrates how directly manipulating local cholesterol levels at the MAM can alter inter-organellar contact sites and suggests that cholesterol buildup at the MAM is the impetus behind the therapeutic benefits of ACAT1/SOAT1 inhibition.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.