LCLAT1

更新于：2025-05-07

基本信息

别名

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

+ [7]

简介

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).

关联

100 项与 LCLAT1 相关的临床结果

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100 项与 LCLAT1 相关的转化医学

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0 项与 LCLAT1 相关的专利（医药）

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项与 LCLAT1 相关的文献（医药）

2025-04-01·Biochemical and Biophysical Research Communications

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

Article

作者: 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.

2025-04-01·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

作者: 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.

2025-04-01·Life Sciences

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

Article

作者: 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.

项与 LCLAT1 相关的新闻（医药）

2023-01-12

·生物谷

Research：中国科学家绘制出发育中心脏的脂质组蓝图

来自中国科学院遗传与发育研究所等机构的科学家们通过研究揭示了发育中的心脏的脂质组蓝图，其或有望帮助揭开心脏结构和代谢成熟背后的动态膜脂质特性。心脏是机体中不可或缺的器官，其具有迷人的发育生物学特性，同时也是发育中的哺乳动物胚胎中第一个发挥作用的器官，心脏中的脂质代谢与心脏的生理学特性之间存在着非常复杂的关联，然而目前研究人员尚未创建出机体心脏器官发生过程中的全面脂质组图谱。近日，一篇发表在国际杂志Research上题为“Lipidome Atlas of the Developing Heart Uncovers Dynamic Membrane Lipid Attributes Underlying Cardiac Structural and Metabolic Maturation”的研究报告中，来自中国科学院遗传与发育研究所等机构的科学家们通过研究揭示了发育中的心脏的脂质组蓝图，其或有望帮助揭开心脏结构和代谢成熟背后的动态膜脂质特性。文章中，研究人员利用高覆盖率的定量脂质组方法构建了小鼠在产前和产后发育阶段的全心脏（862种脂质；31类）和线粒体（587种脂质；27类）的脂质组图谱。研究者发现，随着心脏的发育，二十二碳六烯酸磷脂（docosahexaenoyl-phospholipids）会逐渐形成，而且C18:2, C20:3和C20:4脂肪酰基重塑成为心磷脂的能力也会增强，研究者还注意到，神经酰胺会优先流向鞘磷脂的生物合成，而并不是复杂的糖磷脂的形成。中国科学家绘制出发育中心脏的脂质组蓝图。图片来源：Research (2022). DOI:10.34133/research.0006 利用maSigPro和Gpclust算法，研究人员识别出了448种发育动态脂质的目录，同时还绘制出了550个生物学上相关的发育动态基因文库的基因表达模式。其组合性转录组学和脂质组学方法识别出了Hadha、Lclat1和Lpcat3或能作为一种候选分子驱动子，来分别管理心脏发育过程中的心磷脂和磷脂的动态重塑。研究者的分析结果表明，出生后心脏中心磷脂的重塑构成了一种双相过程，在四亚油酰心磷脂 (tetralinoleoyl cardiolipin, TLCL)形成主要物种之前首先就会积累多不饱和的C78-心磷脂。综上，本文研究结果提供了以脂质为中心的生物学见解，对于后期科学家们理解心脏代谢的灵活性和疾病发生的病理学机制或许非常重要。（生物谷Bioon.com）原始出处： HUAN MIAO,BOWEN LI,ZEHUA WANG, et al. Lipidome Atlas of the Developing Heart Uncovers Dynamic Membrane Lipid Attributes Underlying Cardiac Structural and Metabolic Maturation, Research (2022). DOI: 10.34133/research.0006

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