Ask about this productRelated genes to: ACSL4 antibody
- Gene:
- ACSL4 NIH gene
- Name:
- acyl-CoA synthetase long chain family member 4
- Previous symbol:
- FACL4, MRX63, MRX68
- Synonyms:
- ACS4, LACS4
- Chromosome:
- Xq23
- Locus Type:
- gene with protein product
- Date approved:
- 1997-05-09
- Date modifiied:
- 2017-06-13
Related products to: ACSL4 antibody
Related articles to: ACSL4 antibody
- Glioblastoma (GBM) remains the most lethal primary brain tumor, and the molecular mechanisms driving its aggressiveness are incompletely understood. Recent multi-omics analyses have identified miR-15a-5p as one of the core microRNAs most closely associated with GBM. This study aimed to investigate the functional role and mechanism of miR-15a-5p in GBM pathogenesis. - Source: PubMed
Yu YanyanYuan HelanFang ZikunLiao JinyuanYang YancongLiu JunWei WenjinJiang Qiuhua - Polystyrene nanoplastics (PS-NPs) are emerging food safety contaminants. Ferroptosis is iron-dependent cell death, but its role in PS-NPs hepatotoxicity is unclear. Mice received tail-vein injection of PS-NPs (2-8mg/kg). PS-NPs caused liver injury (elevated transaminases) and possible renal impairment (increased uric acid/creatinine/urea). Hepatic GSH and SOD decreased, IL-1β and TNF-α increased. Mitochondrial shrinkage and cristae loss (ferroptotic features) were observed. PS-NPs upregulated ACSL4, MDA, 4-HNE and TfR, but suppressed FTH1, FPN1, SLC7A11 and GPx4. Thus, ferroptosis mediates PS-NPs liver injury with oxidative stress and inflammation, and PS-NPs may exert multi-organ toxicity. - Source: PubMed
Publication date: 2026/08/29
Ou CiWu HanpengChen YichunYang ZhengtaoWang JingjingZhou Ershun - Pulmonary hypertension (PH) is a life-threatening blood vessel disorder marked by remodeling of the pulmonary arteries. A key feature of this process is the uncontrolled growth of pulmonary artery smooth muscle cells (PASMCs). Although changes in fatty acid metabolism are thought to drive this abnormal cell growth, the exact molecular mechanisms behind it are still not fully understood. - Source: PubMed
Publication date: 2026/08/29
Chen WeiDong YitingShi QihaoMeng HongbingSun JiaweiHan CongmeiYan ChenjieWu ChendongWang JingGeorgescu AdrianaJin KekeYuan Linbo - Ulcerative colitis (UC) is characterized by chronic mucosal inflammation, epithelial injury, oxidative stress, and marked molecular heterogeneity. Ferro-aging has recently been proposed as an ACSL4-associated, iron-dependent aging-related state in primates, but whether its associated transcriptional features are relevant to chronic mucosal inflammatory disease remains unclear. Here, we integrated bulk transcriptomics, machine learning, single-cell RNA sequencing, spatial transcriptomics, and immunohistochemical validation of clinical tissue samples to characterize ferro-aging-related features in UC and identify associated biomarkers. Ferro-aging-related activity was quantified using GSVA and GSEA and was increased in UC, particularly in active disease, with strong associations with inflammatory response, oxidative stress, epithelial injury, and immune-cell infiltration. Transcriptomic stratification further identified a ferro-aging-high state characterized by enhanced inflammatory and tissue-remodeling signatures. WGCNA and LASSO logistic regression generated a five-gene diagnostic model that showed strong performance in the discovery and validation cohorts and was further validated in an independent external cohort (AUC = 0.992, 95% CI 0.979-1.000). Single-cell analysis localized ferro-aging-related activity and prioritized genes mainly to endothelial, fibroblast, and myeloid compartments, while CellChat suggested enhanced myeloid-centered communication involving MIF-CD74/CD44 and collagen-CD44 interactions. Spatial transcriptomics and immunohistochemistry further supported increased CHST15 and MSN expression in UC mucosa. Exploratory candidate-ligand analyses additionally identified Chst15-IN-1 and Polyphyllin VII for future experimental investigation. Collectively, these findings identify CHST15 and MSN as ferro-aging-related biomarkers linking mucosal inflammation, immune-stromal remodeling, and disease-associated tissue organization in UC. - Source: PubMed
Wang QianwenWang NaYan HonglinYuan Jingping - Ferroptosis, an iron-dependent, lipid peroxidation-driven form of regulated cell death, critically contributes to ischemic stroke (IS) pathophysiology through iron overload, glutathione depletion, and dysregulation of the System Xc/GPX4 axis. This review systematically evaluates natural product-derived interventions targeting ferroptosis for IS management. A systematic search of PubMed, Web of Science, and ScienceDirect from their inception through May 22, 2026 identified 74 eligible studies. Our synthesis reveals three core mechanistic hubs: (1) restoring iron homeostasis by regulating ferritinophagy and iron transporters; (2) suppressing lipid peroxidation by targeting the ACSL4/LPCAT3 cascade and activating Nrf2/HO-1 signaling; and (3) reinforcing antioxidant defenses through upregulation of the System Xc/GSH/GPX4 pathway. The reviewed interventions encompass six major classes of natural products-including flavonoids, terpenoids, saponins, phenolic acids, phenylpropanoids, and alkaloids-and multi-herb formulas such as Buyang Huanwu Decoction and Naotaifang. Collectively, these agents reduce malondialdehyde (MDA) levels while elevating superoxide dismutase (SOD) and glutathione (GSH) activities in preclinical models. Crucially, we identify persistent translational bottlenecks, including poor pharmacokinetic profiles, undefined blood-brain barrier permeability, uncharacterized active constituents in herbal formulas, and a distinct lack of clinical validation. These findings establish that while natural compounds robustly inhibit ferroptosis in experimental models, bridging the translational gap requires rigorous standardization and high-quality clinical trials to fulfill their therapeutic potential. - Source: PubMed
Publication date: 2026/08/24
Li JunLi ZhongshaLi ChengcongLiu YongpingJing XingwenZhu FengJin WeiLv Chao