LIMA1

Last update 08 May 2025

Basic Info

Synonyms

Epithelial protein lost in neoplasm, EPLIN, LIM domain and actin binding 1

+ [3]

Introduction

Actin-binding protein involved in actin cytoskeleton regulation and dynamics. Increases the number and size of actin stress fibers and inhibits membrane ruffling. Inhibits actin filament depolymerization. Bundles actin filaments, delays filament nucleation and reduces formation of branched filaments (PubMed:12566430). Acts as a negative regulator of primary cilium formation (PubMed:32496561). Plays a role in cholesterol homeostasis. Influences plasma cholesterol levels through regulation of intestinal cholesterol absorption. May act as a scaffold protein by regulating NPC1L1 transportation, an essential protein for cholesterol absorption, to the plasma membrane by recruiting MYO5B to NPC1L1, and thus facilitates cholesterol uptake (By similarity).

100 Clinical Results associated with LIMA1

100 Translational Medicine associated with LIMA1

0 Patents (Medical) associated with LIMA1

107

Literatures (Medical) associated with LIMA1

01 Dec 2025·Current Atherosclerosis Reports

From Genetic Findings to new Intestinal Molecular Targets in Lipid Metabolism

Review

Author: Ducheix, Simon ; Rimbert, Antoine ; Cariou, Bertrand ; Le May, Cédric

PURPOSE OF REVIEWWhile lipid-lowering therapies demonstrate efficacy, many patients still contend with significant residual risk of atherosclerotic cardiovascular diseases (ASCVD). The intestine plays a pivotal role in regulating circulating lipoproteins levels, thereby exerting influence on ASCVD pathogenesis. This review underscores recent genetic findings from the last six years that delineate new biological pathways and actors in the intestine which regulate lipid-related ASCVD risk.RECENT FINDINGSSpecifically, we detail the role of LIMA1 in cholesterol absorption within enterocytes, the function of PLA2G12B in the expansion and lipidation of chylomicrons, the involvement of SURF4 in lipoprotein secretion, and the discovery of a gut-derived hormone named CHOLESIN that modulates cholesterol homeostasis through GPR146 via a gut-liver crosstalk. We further discuss the potential of these newly identified genes and pathways as novel targets for pharmaceutical intervention. Newly identified genetic and intestinal molecular mechanisms offer promising opportunities for preventing and treating ASCVD, but careful evaluation and further research are needed to optimize their clinical application.

01 Apr 2025·Advanced Science

LIMA1 O‐GlcNAcylation Promotes Hepatic Lipid Deposition through Inducing β‐catenin‐Regulated FASn Expression in Metabolic Dysfunction‐Associated Steatotic Liver Disease

Article

Author: Zheng, Guojun ; Yang, Fuji ; Yan, Yongmin ; Gu, Kefeng ; Fan, Lin ; Li, Tingfen ; Chen, Yifei ; Zhu, Ling

AbstractHepatic lipid deposition is a key factor in progressing metabolic dysfunction‐associated steatotic liver disease (MASLD). This study investigates the impact of the LIM domain and actin‐binding protein 1 (LIMA1) on hepatic steatotic in MASLD and explore the underlying mechanisms. Increased levels of LIMA1 is observed in both serum and serum sEV of metabolic dysfunction‐associated steatohepatitis (MASH) patients compared to healthy controls, with AUROC values of 0.76 and 0.86, respectively. Furthermore, increased LIMA1 O‐GlcNAcylation is observed in mouse models of MASLD, and steatotic hepatocytes. Mechanistic studies revealed that steatosis upregulated Host cell factor 1 (HCF1) and O‐GlcNAc transferase (OGT) expression, leading to catalyzed O‐GlcNAcylation at the T662 site of LIMA1 and subsequent inhibition of its ubiquitin‐dependent degradation. O‐GlcNAcylation of LIMA1 enhances hepatocyte lipid deposition by activating β‐catenin/FASn‐associated signaling. Additionally, compared with their AAV8‐TBG‐LIMA1‐WT counterparts, AAV8‐TBG‐LIMA1ΔT662 injection exhibited decreases in systemic insulin resistance, steatosis severity, inflammation and fibrosis in HFD‐fed and CDAHFD‐fed LIMA1 HKO (hepatocyte‐specific knockout) mice. Moreover, LTH‐sEV‐mediated delivery of LIMA1 promoted MASLD progression by promoting hepatic stellate cell (HSC) activation. The findings suggest that serum sEV LIMA1 may be a potential noninvasive biomarker and therapeutic target for individuals with MASH.

01 Jan 2025·Experimental Neurology

DDAH1 deficiency exacerbates cerebral vascular endothelial dysfunction by aggravating BBB disruption and oxidative stress in thoracic blast-induced brain injury

Article

Author: Hou, Mingxiao ; Tong, Changci ; Mao, Shun ; Cong, Peifang ; Liu, Yunen ; Shi, Lin

As terrorist incidents and underground explosion events have become more frequent around the world, brain injury caused by thoracic blast exposure has been more highlighted due to its injured organ, subsequent social and economic burden. It has been reported dimethylarginine dimethylaminohydrolase 1 (DDAH1) plays important roles in regulating vascular endothelial injury repair and angiogenesis, but its role in thoracic blast-induced brain injury remains to be explained. This study seeks to investigate the mechanism of DDAH1 on thoracic blast-induced brain injury. 40 C57BL/6 wild type mice and 40 DDAH1 knockout mice were randomly and equally divided into control group and blast group, respectively. The integrity of blood-brain barrier (BBB) was detected by Evans blue test. The serum inflammatory factors, nitric oxide (NO) contents, and asymmetric dimethylarginine (ADMA) levels were determined through ELISA. HE staining and reactive oxygen species (ROS) detection were performed for histopathological changes. Western blot was used to detect the proteins related to oxidative stress, tight junction, focal adhesion, vascular endothelial injury, and the DDAH1/ADMA/eNOS signaling pathway. DDAH1 deficiency aggravated thoracic blast-induced BBB leakage, inflammatory response, and the increased levels of inflammatory-related factors. Additionally, DDAH1 deficiency also increased ROS generation, MDA and IRE-α expression. Regarding cerebral vascular endothelial dysfunction, DDAH1 deficiency increased the expression of MCAM, FN1, LIMK1, VEGF, MMP9, Vimentin and N-cadherin, while lowering the expression of FMR1, Occludin, claudin-3, claudin-5, Lyn, LIMA1, Glrb, Sez6, Dystrophin, and phosphorylation of VASP. Also, DDAH1 deficiency exacerbated explosion-induced increase of ADMA and decrease of eNOS activity and NO contents. Thus, we conclude that DDAH1 could prevent cerebral vascular endothelial dysfunction and related injury by inhibiting ADMA signaling and increasing eNOS activity in thoracic blast induced brain injury.

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LIMA1

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