AACS

Last update 08 May 2025

Basic Info

Synonyms

AACS, acetoacetyl-CoA synthetase, ACSF1

+ [4]

Introduction

Converts acetoacetate to acetoacetyl-CoA in the cytosol (By similarity). Ketone body-utilizing enzyme, responsible for the synthesis of cholesterol and fatty acids (By similarity).

100 Clinical Results associated with AACS

100 Translational Medicine associated with AACS

0 Patents (Medical) associated with AACS

364

Literatures (Medical) associated with AACS

01 May 2025·Pharmacological Research

Breaking the synergism of iron overload and miR-122 to rescue lipid accumulation and peroxidation in MASLD

Article

Author: Wu, Chenghua ; Gao, Zelong ; Chai, Yifeng ; Sun, Yan ; Zhang, Hongwei ; Shen, Hui ; Wang, Weili ; Yang, Jianxin ; Wu, Mengpu ; Qian, Jianxin ; Tang, Yuxiao ; Wang, Dongyao ; Li, Min ; Li, Chenqi ; Xie, Feng ; Wu, Huiwen

MASLD is a multifactorial disease with specific subtypes being featured by hepatic iron overload and loss of miR-122, a liver-specific microRNA regulating hepatic lipid homeostasis. Previously we reported the mechanism of iron overload decreasing miR-122. Interestingly, we found that mice lacking miR-122 were highly sensitive to iron overload-induced steatosis and fibrosis. The present study aimed to disclose the downstream mechanisms and the preventive measures targeting miR-122. We first validated the decreases in iron-related genes and miR-122 in MASLD. By using LC-MS/MS and gas-chromatography, we found that the combination of miR-122 knockout and iron overload significantly increased the production and peroxidation of polyunsaturated fatty acids (PUFAs). However, miR-122 knockout itself only incurred lipid accumulation, suggesting a synergistic effect of miR-122 knockout and iron overload in lipid peroxidation. We then located the key enzymes involved in PUFA production and peroxidation by the transcriptome and proteome analysis. Mechanistically, miR-122 and iron regulated fatty acid synthesis through Aacs, fatty acid desaturation through Fads2, and PUFAs oxidation through CYPs. Re-supplementation of miR-122 by recombinant adeno-associated virus or agomir effectively broke the synergism of miR-122 knockout and iron overload in vivo. We further designed a miR-122 expression reporter cell model for high-throughput screening on 2543 natural compounds, and eventually found and validated that the dihydroberberine could upregulate miR-122 expression and correct iron overload-induced lipid disorders. These results identified the synergistic role of miR-122 and iron in PUFAs production and peroxidation, and also proposed the potential application of dihydroberberine as a preventive and therapeutic candidate for MASLD.

01 Mar 2025·Biochemistry and Biophysics Reports

RNA-seq analysis reveals transcriptome changes in livers from Efcab4b knockout mice

Article

Author: Pedicini, Lucia ; McKeown, Lynn ; Forde, Niamh ; Smith, Jessica ; Alcala, Cintli Morales ; Murray, Ryan D ; Cheng, Chew W ; Deligianni, Fenia ; Todd, Harriet J

EFCAB4B is an evolutionarily conserved protein that encodes for the Rab GTPase Rab46, and the CRAC channel modulator, CRACR2A. Previous genome wide association studies have demonstrated the association of EFCAB4B variants in the progression of non-alcoholic fatty liver disease (NAFLD). In this study we show that mice with global depletion of Efcab4b ^-/- have significantly larger livers than their wild-type (WT) counterparts. We performed RNA-sequencing (RNA-seq) analysis of liver tissues to investigate differential global gene expression among Efcab4b ^-/- and WT mice. Of the 69 differentially expressed genes (DEGs), analyses of biological processes found significant enrichment in liver and bile development, with 6 genes (Pck1, Aacs, Onecut1, E2f8, Xbp1, and Hes1) involved in both processes. Specific consideration of possible roles of DEGs or their products in NAFLD progression to (NASH) and hepatocarcinoma (HCC), demonstrated DEGs in the livers of Efcab4b ^-/- mice had roles in molecular pathways including lipid metabolism, inflammation, ER stress and fibrosis. The results in this study provide additional insights into molecular mechanisms responsible for increasing susceptibility of liver injuries associated with EFCAB4B.

01 Feb 2025·Journal of Pharmaceutical and Biomedical Analysis

Proteomics exploration of metformin hydrochloride for diabetic kidney disease treatment via the butanoate metabolism pathway

Article

Author: Qiu, Shi ; Wang, Xian ; Cai, Ying ; Zhang, Aihua ; Guo, Sifan ; Chen, Hongwei ; Wang, Yan ; Chai, Jinxuan ; Wang, Zhibo ; Xie, Dandan ; Wang, Shiwei ; Hu, Zhencai

Diabetic nephropathy (DKD) is a diabetesrelated kidney injury with an increasing incidence every year. Metformin hydrochloride (MET), a cornerstone treatment for glucose lowering, has been widely reported for the treatment of DKD, but the specific molecular mechanisms and potential therapeutic targets still need to be further explored. We used kidney tissues from db/db mice as samples and used proteomics and bioinformatics to analyse the function, distribution and related pathways of differential proteins in DKD, focusing on the assessment of the binding energies of key proteins in the butyrate pathway and drugs at the molecular level, which showed that the expression profiles of differential proteins in kidney tissues were altered after MET treatment, involving energy metabolism. The key proteins involved in the butanoate metabolism pathway, including AACS, ACSM3, EHHADH and HMGCS2, exhibit binding energies to MET of ＜-5 kcal. It is therefore plausible that MET treatment may affect the butanoate metabolism pathway, potentially ameliorating the progression of DKD by modulating mitochondrial function and inflammatory responses.

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