ArticleBiology direct2023
ACSM5 inhibits ligamentum flavum hypertrophy by regulating lipid accumulation mediated by FABP4/PPAR signaling pathway.
Article in Biology direct, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 18 citations in OpenAlex.
- PPARγ signalling pathway: molecular mechanisms and therapeutic potential in ligamentum flavum hypertrophy and lumbar spinal stenosis.Journal of translational medicine · 2026Review
- Distinct damage levels and transcriptional responses of lung in Hezuo pigs and Bama pigs during cold exposure.Animal bioscience · 2026Article
- Plasma Metabolic Signature and Single-Cell Regulatory Network for Ischemic Stroke.Translational stroke research · 2026Article
- ACSM5 c.1273 C> A Polymorphism Promotes Malignant Progression of Lung Adenocarcinoma in Xuanwei Region.Applied biochemistry and biotechnology · 2026Article
- Integrating WGCNA and machine learning algorithm to identify ACSM5 as a prognostic biomarker and therapeutic target for predicting immunotherapy efficacy in non-small cell lung cancer.Translational cancer research · 2026Article
- METTL14 and WTAP play a crucial role in the regulation of bovine preadipocyte differentiation.Animal biotechnology · 2025Article
- Ligamentum flavum: changes in vascular density, physical and histopathobiochemical properties in lumbar spine based on anatomical localization, spinal segment levels, and presence of lumbar spinal stenosis.North American Spine Society journal · 2025Article
- ACSM5 Regulates Ferroptosis in Hepatocellular Carcinoma by Up-Regulating POR and Modulating Lipid Metabolism.Cancer science · 2025Article
- Curcumin-loaded nanoparticles for renal ischemia-reperfusion injuries: Triple-play of redox homeostasis accommodation, lipid metabolism regulation, and nuclear magnetic tracing.Materials today. Bio · 2025Article
- Loss of SVIP Results in Metabolic Reprograming and Increased Retention of Very-Low-Density Lipoproteins in Hepatocytes.International journal of molecular sciences · 2025Article
- Key genes and processes affected by atorvastatin treatment in mouse diaphragm muscle.Archives of toxicology · 2025Article
- Nanomaterial-Mediated Reprogramming of Macrophages to Inhibit Refractory Muscle Fibrosis.Advanced materials (Deerfield Beach, Fla.) · 2024Article
- Unveiling therapeutic targets for spinal stenosis from genetic insights: a Mendelian randomization analysis.Scientific reports · 2024Article
- Cellular and Molecular Mechanisms of Hypertrophy of Ligamentum Flavum.Biomolecules · 2024Review
- RMRP accelerates ligamentum flavum hypertrophy by regulating GSDMD-mediated pyroptosis through Gli1 SUMOylation.Frontiers in immunology · 2024Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundLigamentum flavum (LF) hypertrophy is the main cause of lumbar spinal canal stenosis (LSCS). Previous studies have shown that LF hypertrophy tissue exhibits abnormal lipid accumulation, but the regulatory mechanism remains unclear. The objective of this study was to explore the function and potential mechanism of ACSM5 in LF lipid accumulation.
methodsTo assess the ACSM5 expression levels, lipid accumulation and triglyceride (TG) level in LF hypertrophy and normal tissue, we utilized RT-qPCR, western blot, oil red O staining, and TG assay kit. The pearson correlation coefficient assay was used to analyze the correlation between ACSM5 levels and lipid accumulation or TG levels in LF hypertrophy tissue. The role of ACSM5 in free fatty acids (FFA)-induced lipid accumulation in LF cells was assessed in vitro, and the role of ACSM5 in LF hypertrophy in mice was verified in vivo. To investigate the underlying mechanisms of ACSM5 regulating lipid accumulation in LF, we conducted the mRNA sequencing, bioinformatics analysis, and rescue experiments.
resultsIn this study, we found that ACSM5, which was significantly down-regulated in LF tissues, correlated with lipid accumulation. In vitro cell experiments demonstrated that overexpression of ACSM5 significantly inhibited FFA-induced lipid accumulation and fibrosis in LF cells. In vivo animal experiments further confirmed that overexpression of ACSM5 inhibited LF thickening, lipid accumulation, and fibrosis. Mechanistically, ACSM5 inhibited lipid accumulation of LF cells by inhibiting FABP4-mediated PPARγ signaling pathway, thereby improving hypertrophy and fibrosis of LF.
conclusionsour findings elucidated the important role of ACSM5 in the regulation of LF lipid accumulation and provide insight into potential therapeutic interventions for the treatment of LF hypertrophy. This study further suggested that therapeutic strategies targeting lipid deposition may be an effective potential approach to treat LF hypertrophy-induced LSCS.
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