ArticleJournal of translational medicine2024
ACACA reduces lipid accumulation through dual regulation of lipid metabolism and mitochondrial function via AMPK- PPARα- CPT1A axis.
Article in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 99 citations in OpenAlex.
- A mature tertiary lymphoid structure-associated spatial niche is inversely associated with ACC1-related lipid metabolism in neoadjuvant-treated hepatocellular carcinoma.Translational oncology · 2026Article
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- Effects of SIRT7 Inhibition on Milk Fat Synthesis and Fatty Acid Composition in Dairy Goat Mammary Epithelial Cells.Animals : an open access journal from MDPI · 2026Article
- Occupational-circadian disruption and physical inactivity conjointly amplify fatty liver risk: based on liver ultrasound transient elastography.International journal of occupational medicine and environmental health · 2026Article
- Psoralen enhances direct cardiac reprogramming via activating PPARα and driving mitochondrial fission and improves cardiac function after myocardial infarction.Stem cell research & therapy · 2026Article
- Gene co-expression networks related to intramuscular fatty acid composition across different pig genotypes.BMC genomics · 2026Article
- Activation of PPARγ and CPT1A Mediates the Hepatoprotective Effect of Ginsenoside CK against NAFLD in Rats.Biological procedures online · 2026Article
- PKCβ II antagonizes O-GlcNAcylated FOXO4 and inhibits lipid synthesis.Apoptosis : an international journal on programmed cell death · 2026Article
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- Targeting the ASB3-CPT1A axis-a new player in combating metabolic dysfunction-associated steatotic liver disease: Editorial on "Hepatocytic ankyrin repeat and SOCS box protein 3 deficiency alleviates metabolic dysfunction-associated steatotic liver disease by decreasing ubiquitin-mediated carnitine palmitoyltransferase 1A".Clinical and molecular hepatology · 2026Article
- Metabolic dysfunction-associated steatotic liver disease: On track to become the dominant etiology of hepatocellular carcinoma: Reply to correspondence on "Downregulation of the MARC1 p.A165 risk allele reduces hepatocyte lipid content by increasing beta-oxidation".Clinical and molecular hepatology · 2026Article
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- Targeting amino acid metabolic pathways: a novel therapeutic strategy for hyperuricemia-associated complications.Amino acids · 2026Review
- High-fat diet leads to male reproductive dysfunction by disrupting lipid-droplet-mediated organelle crosstalk.Cellular & molecular biology letters · 2026Article
- Choline Deficiency Drives the Inflammation-Fibrosis Cascade: A Spatiotemporal Atlas of Hepatic Injury from Weeks 6 to 10.Antioxidants (Basel, Switzerland) · 2026Article
- 1,1-Diethoxyethane increases insulin sensitivity and ameliorates obesity and dyslipidemia in mice fed high-fat diet.npj metabolic health and disease · 2026Article
- Xanthine oxidoreductase activity in MASLD: links to lipid metabolism, oxidative stress, and inflammation.Frontiers in endocrinology · 2026Article
- Qingyi Decoction Alleviates Alcoholic Pancreatitis by Improving Glycerolipid Homeostasis via the AMPK/SREBP-1c/PPARα Pathway.Journal of inflammation research · 2026Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundNon-alcoholic fatty liver disease (NAFLD) is a multifaceted metabolic disorder, whose global prevalence is rapidly increasing. Acetyl CoA carboxylases 1 (ACACA) is the key enzyme that controls the rate of fatty acid synthesis. Hence, it is crucial to investigate the function of ACACA in regulating lipid metabolism during the progress of NAFLD.
methodsFirstly, a fatty liver mouse model was established by high-fat diet at 2nd, 12th, and 20th week, respectively. Then, transcriptome analysis was performed on liver samples to investigate the underlying mechanisms and identify the target gene of the occurrence and development of NAFLD. Afterwards, lipid accumulation cell model was induced by palmitic acid and oleic acid (PA ∶ OA molar ratio = 1∶2). Next, we silenced the target gene ACACA using small interfering RNAs (siRNAs) or the CMS-121 inhibitor. Subsequently, experiments were performed comprehensively the effects of inhibiting ACACA on mitochondrial function and lipid metabolism, as well as on AMPK- PPARα- CPT1A pathway.
resultsThis data indicated that the pathways significantly affected by high-fat diet include lipid metabolism and mitochondrial function. Then, we focus on the target gene ACACA. In addition, the in vitro results suggested that inhibiting of ACACA in vitro reduces intracellular lipid accumulation, specifically the content of TG and TC. Furthermore, ACACA ameliorated mitochondrial dysfunction and alleviate oxidative stress, including MMP complete, ATP and ROS production, as well as the expression of mitochondria respiratory chain complex (MRC) and AMPK proteins. Meanwhile, ACACA inhibition enhances lipid metabolism through activation of PPARα/CPT1A, leading to a decrease in intracellular lipid accumulation.
conclusionTargeting ACACA can reduce lipid accumulation by mediating the AMPK- PPARα- CPT1A pathway, which regulates lipid metabolism and alleviates mitochondrial dysfunction.
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Registered trials
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.