ACOT1
- Known as:
- ACOT1
- Catalog number:
- 001016A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ACOT1
Related genes to: ACOT1
- Gene:
- ACOT1 NIH gene
- Name:
- acyl-CoA thioesterase 1
- Previous symbol:
- -
- Synonyms:
- ACH2, CTE-1, LACH2
- Chromosome:
- 14q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 2006-08-30
- Date modifiied:
- 2014-11-18
Related products to: ACOT1
Related articles to: ACOT1
- Sepsis associated acute liver injury is a major contributor to multiple organ dysfunction and mortality in critically ill patients. ACOT1 has emerged as a promising therapeutic target, demonstrated to inhibit disseminated intravascular coagulation through its anti-ferroptosis activity. However, its specific function and mechanistic role in the context of during endotoxemia-induced liver injury have not been elucidated. This study demonstrates that ferroptosis was markedly activated in both lipopolysaccharide (LPS)-stimulated AML12 hepatocytes and LPS-induced acute liver injury mouse models. RNA sequencing and bioinformatics analyses identified ACOT1 as the most significantly downregulated genes following LPS stimulation. Functionally, ACOT1 overexpression upregulated GPX4 and SLC7A11 expression, reduced mitochondrial ROS and Fe accumulation, which ultimately attenuated LPS-induced hepatocyte ferroptosis. Mechanistically, ACOT1 overexpression activated PPARγ, thus suppressing NF-κB pathway activation and inflammatory responses thereafter. IP-MS and immunofluorescence staining confirmed that SLC25A5 interacts with ACOT1 and functions as a molecular partner in regulating hepatocyte ferroptosis by reducing mitochondrial ROS and Fe levels. Protein interaction analysis between ACOT1 and SLC25A5 showed a Rosetta score of -271.16 kcal/mol, indicating strong binding affinity. Collectively, our results identified ACOT1 as a novel inhibitor of ferroptosis in LPS-induced acute liver injury. ACOT1 exerts protective effects by modulating the PPARγ/NF-κB signaling axis and cooperating with SLC25A5 to regulate oxidative stress-driven ferroptosis. These results highlight ACOT1 as a potential regulator for inflammatory liver injury. - Source: PubMed
Publication date: 2026/08/01
Xu ChengzhuWang ShunWang XiyangZhang XuanOuyang SuxiaHuang TingxuanJin DanqunZhang LeXu Yuanyuan - Diabetic cardiomyopathy (DCM) is a critical pathological driver of heart failure in diabetic patients, primarily characterized by progressive myocardial fibrosis. Nevertheless, the core molecular network linking upstream metabolic dysregulation to the aberrant activation of downstream cardiac fibroblasts remains largely elusive. In this study, we combined in vivo and in vitro approaches with bioinformatics analysis. A high-fat diet-induced mouse model of diabetic myocardial fibrosis was established, and transcriptome sequencing was performed to screen for hub genes, which were subsequently validated in two independent DCM datasets. Single-cell RNA sequencing revealed that PDK4 and ACOT1 were upregulated in cardiac fibroblasts under pathological conditions. In vitro experiments confirmed that high glucose induced the expression of PDK4, ACOT1, and fibrotic markers in human primary cardiac fibroblasts. Molecular docking predicted a potential interaction between PDK4 and ACOT1. Collectively, our findings identify PDK4 and ACOT1 as evolutionarily conserved metabolic hub genes associated with myocardial fibrosis in DCM, suggesting a putative "metabolism-fibrosis axis" and providing potential therapeutic targets. - Source: PubMed
Liu HuanQi GuanmingOuyang ShengrongMa Feifei - As a fat-soluble vitamin, vitamin E (VE) is prone to suboptimal intake in the general population. Alpha-tocopherol (α-TE) represents the most biologically significant form of VE in vivo. Nevertheless, the potential detrimental effects of α-TE deficiency on health remain unclear. This study was conducted to investigate the effect of α-TE deficiency on hepatic metabolism and gut microbiota. C57BL/6J mice were randomly assigned to receive one of three dietary regimens: a α-TE-deficient diet, a control diet with normal α-TE, or a high-dose diet containing four times the normal α-TE level. Histopathology, serum biochemistry, RNA-Seq, RT-qPCR, Western blot, and 16S rRNA gene sequencing with correlation analysis were used to assess metabolic phenotypes, hepatic circadian, hepatic lipid metabolism, and cecal microbiota, respectively. The results demonstrated that α-TE deficiency induced hepatic steatosis and lipid metabolic disturbances. α-TE deficiency significantly decreased Arntl and Clock expression, but increased Per2. Additionally, it upregulated the expression of lipogenic genes such as , and and simultaneously downregulated fatty acid oxidation genes such as , and , bringing about imbalance in lipid homeostasis. In addition, α-TE deficiency greatly changed the structure and composition of gut microbiota. Bacterial genera like , , , , and were significantly correlated with hepatic circadian and lipid metabolism gene expression with the strongest correlation being . This work is the first to reveal that short term α-TE deficiency could cause lipid metabolic disorder via the "gut microbiota-liver circadian clock" axis, which provides novel insights into the etiology of nutrition-related metabolic diseases and targets for nutritional intervention. - Source: PubMed
Publication date: 2026/06/09
Peng LeiZhao YanFan YuqinPeng QiSheng JunTian YangGao Xiaoyu - Diabetic cardiomyopathy (DCM) is characterized by metabolic dysfunction and lipotoxicity. The roles of acyl-CoA thioesterase 1 (ACOT1) and the novel post-translational modification lactylation in its pathogenesis remain unclear. This study aimed to investigate the stage-specific function of ACOT1 and the mechanism by which lactylation of SREBP1c regulates lipid metabolism in DCM. - Source: PubMed
Publication date: 2026/06/06
Liao ZeyuFu YahuiLi Ran - Metabolic dysfunction-associated steatotic liver disease (MASLD) represents a leading global health burden, yet its diagnosis and staging rely heavily on invasive liver biopsies. Liquid biopsy, utilizing circulating cell-free DNA (cfDNA), offers a promising noninvasive alternative to capture hepatic genomic instability. This review consolidates current knowledge on cfDNA biomarkers in MASLD, moving from established quantitative metrics to emerging epigenetic insights. The role of mitochondrial DNA copy number (mtDNAcn) is examined as a dynamic marker of oxidative stress, highlighting its biphasic response: compensatory upregulation in early disease versus depletion in advanced fibrosis. Furthermore, key nuclear copy number variations (CNVs) specifically the XPO4 duplication (13q12.11), CES1 deletion (16q12.2), and ACOT1 deletion (14q24.3) are discussed regarding their mechanistic drivers of fibrogenesis and lipid metabolism dysregulation. Addressing the complexity of MASLD pathogenesis, the discussion extends to emerging multi-modal metrics, including DNA methylation and fragmentomics. These modalities offer superior specificity by tracing the "tissue of origin" and distinguishing apoptotic from necrotic fragmentation patterns, effectively addressing the diagnostic challenges posed by the "burnout" phenomenon in advanced cirrhosis. Finally, critical future directions are outlined, emphasizing the necessity for standardized pre-analytical protocols and the integration of multi-omics data with machine learning. This comprehensive approach will shed light on the transition cfDNA from a research tool to a precise clinical instrument for early risk stratification and therapeutic monitoring. - Source: PubMed
Publication date: 2026/05/02
Lim Wei-YueMohamed RosmawatiPung Yuh-FenZain Shamsul Mohd