LCLAT1

Last update 08 May 2025

Basic Info

Synonyms

1-acylglycerol-3-phosphate O-acyltransferase 8, 1-AGP acyltransferase 8, 1-AGPAT 8

+ [7]

Introduction

Exhibits acyl-CoA:lysocardiolipin acyltransferase (ALCAT) activity; catalyzes the reacylation of lyso-cardiolipin to cardiolipin (CL), a key step in CL remodeling (By similarity). Recognizes both monolysocardiolipin and dilysocardiolipin as substrates with a preference for linoleoyl-CoA and oleoyl-CoA as acyl donors (By similarity). Also exhibits 1-acyl-sn-glycerol-3-phosphate acyltransferase activity (AGPAT) activity; converts 1-acyl-sn-glycerol-3- phosphate (lysophosphatidic acid or LPA) into 1,2-diacyl-sn-glycerol-3- phosphate (phosphatidic acid or PA) by incorporating an acyl moiety at the sn-2 position of the glycerol backbone (PubMed:16620771). Possesses both lysophosphatidylinositol acyltransferase (LPIAT) and lysophosphatidylglycerol acyltransferase (LPGAT) activities (PubMed:19075029). Required for establishment of the hematopoietic and endothelial lineages (By similarity).

100 Clinical Results associated with LCLAT1

100 Translational Medicine associated with LCLAT1

0 Patents (Medical) associated with LCLAT1

Literatures (Medical) associated with LCLAT1

01 Apr 2025·Biochemical and Biophysical Research Communications

Liraglutide modulates ALCAT1-Mediated cardiolipin remodeling to improve cardiac function in obese mice

Article

Author: Wang, Yan ; Zhou, Xinli ; Shi, Yingzhou ; Hu, Tingting ; Wang, Lulu ; Xuan, Qiuhui ; Zhang, Ruxuan

Obesity, a significant risk factor for cardiovascular diseases, induces cardiolipin (CL) remodeling. Acyl-CoA:lysocardiolipin acyltransferase-1 (ALCAT1), a key enzyme in CL metabolism, drives mitochondrial impairment and cardiac dysfunction in obesity. Although glucagon-like peptide-1 receptor agonists (GLP-1RAs) exhibit cardioprotective properties, their effects on ALCAT1-mediated CL remodeling in obesity-induced myocardial injury remain unclear. Male C57BL/6 mice fed a high-fat diet (HFD) or standard diet (STD) for 12 weeks received liraglutide (200 μg/kg/day) or saline during the last 4 weeks. Cardiac function was evaluated by echocardiography; CL content was quantified using LC-MS, and myocardial alterations were assessed through histological and protein analyses. In HFD-fed mice, cardiac lipid accumulation, left ventricular hypertrophy, and myocardial collagen deposition were observed. Additionally, these mice exhibited reduced CL content, altered CL aliphatic chain composition, and upregulated ALCAT1 expression. In contrast, liraglutide treatment significantly increased total CL content, modified CL acyl chain composition, and downregulated ALCAT1 expression. Mechanistically, liraglutide activated the PI3K/AKT pathway via GLP-1 receptor signaling, attenuated oxidative stress markers (3-nitrotyrosine, Rac1 activation), and improved mitochondrial dynamics by reducing DRP1-mediated fission. These results demonstrate that liraglutide mitigates obesity-induced cardiac dysfunction by suppressing ALCAT1-driven CL remodeling, enhancing mitochondrial homeostasis, and reducing oxidative stress. This study elucidates the cardioprotective mechanisms of liraglutide and highlights its therapeutic potential for obesity-related cardiomyopathy.

01 Apr 2025·Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids

Lipid metabolism associated PLPP4 gene drives oncogenic and adipogenic potential in breast cancer cells

Article

Author: Makwana, Sweta H ; Mandal, Chandi C ; Kumari, Monika ; Soni, Sneha ; Bansal, Shivani

Lipid metabolic reprogramming plays a pivotal role in cancer cell evolution and causing subsequent cancer growth, metastasis and therapy resistance. Cancer associated adipocyte and/or cancer derived adipocyte-like cells often supply fuels and various factors to fulfill the cells bioenergetics to enhance oncogenic potential. This study intends to find out a set of dysregulated genes involved in lipid metabolism in breast cancer studies and uncovers the role of unexplored dysregulated gene in cancer potential. Cancer database analysis determines seven seed signature genes (PLPP2, PLPP4, CDS1, ASAH2, LCLAT1, LPCAT1 and LASS6/CERS6) concluded from relative expression and survival analysis. Furthermore, experimental analysis unveils the gene PLPP4 (Phospholipid Phosphatase 4) as oncogene confirmed by knockdown and overexpression studies in MDA-MB 231 and MCF-7 breast cancer cells. PLPP4 enzyme is involved in regulation of triacyl glycerol metabolism. Lipid accumulation along with other studies documented enhanced lipid droplets, TAG formation and glycerol release with concomitant increased expressions of various adipogenic markers (e.g., PPARγ, perilipin 1 and leptin) in breast cancer cells transfected with PLPP4 gene expressing plasmid whereas downregulation of PLPP4 gene diminished lipid accumulation and adipocyte marker gene expressions. Our findings also revealed that BMP2 induced adipogenic potential in breast cancer cells was mitigated in response to downregulation of PLPP4 gene expression. All these findings together, for first time, demonstrated that BMP2 drives PLPP4 to enhance both oncogenic and adipogenic potential in breast cancer cells. This article uncovers the perturbed lipid metabolism associated PLPP4 acts as oncogene presumably by modulating adipogenic activity in cancer cells.

01 Apr 2025·Life Sciences

Lack of ALCAT1 enhances the protective effects of aerobic exercise on kidney in HFpEF mice

Article

Author: Liu, Renhan ; Zhang, Lili ; Tian, Zhenjun ; Geng, Yanbin ; Xi, Yue ; Zhao, Yifang ; Ma, Yixuan ; Feng, Lili ; Bo, Wenyan

AIMSHeart failure with preserved ejection fraction (HFpEF) is an increasingly prevalent cardiovascular disease, which is often accompanied by kidney dysfunction. Exercise has been recognized as a feasible strategy to improve renal function. The aim of this study was to investigate whether aerobic exercise (AE) could ameliorate HFpEF-induced renal injury by regulating the expression of acyl-coenzyme A: lysocardiolipin acyltransferase-1 (ALCAT1).MATERIALS AND METHODSEight-week-old C57BL/6 and Alcat1 knockout mice were used to establish a HFpEF induced kidney injury model. Mice in the exercise-intervention group were performed a six-week of AE training. Cardiac function and blood pressure were assessed using echocardiography and a non-invasive intelligent blood pressure monitor. Renal morphology and function were detected by HE, Masson, and PAS staining, as well as biochemical assays using commercial kits. Oxidative stress, inflammation, apoptosis, and renal fibrosis-related proteins were detected by Western Blotting.KEY FINDINGSIn the HFpEF induced kidney injury model, ALCAT1 protein expression was upregulated, accompanied by cardiac and renal dysfunction. These pathological changes were reversed by AE. In addition, Alcat1 knockout significantly alleviated HFpEF-induced oxidative stress, inflammation, apoptosis, and fibrosis in the kidneys. Furthermore, Alcat1 knockout further enhanced the protective effects of exercise, ameliorating renal injury and improving renal function in HFpEF mice.SIGNIFICANCEAE significantly improved renal function by alleviating oxidative stress, inflammation, apoptosis, and fibrosis in HFpEF mice. These beneficial effects were further enhanced in the lack of ALCAT1. Thus, ALCAT1 might represent a potential therapeutic target for the treatment of HFpEF-induced kidney injury.

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LCLAT1

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