ACSL4
- Known as:
- ACSL4
- Catalog number:
- 001047A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ACSL4
Related genes to: ACSL4
- 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
Related articles to: ACSL4
- Periodontitis represents one of the most prevalent chronic inflammatory diseases, characterized by progressive periodontal tissue destruction driven by immune dysregulation. Emerging evidence establishes ferroptosis-an iron-dependent, lipid-peroxidation-driven form of regulated cell death-as a pivotal but underexplored driver of the pathological "cell death-inflammation-re-death" cycle in periodontitis. Ferroptotic cells release damage-associated molecular patterns (DAMPs) including oxidized lipids, HMGB1, and iron species that amplify inflammation. The spatiotemporal heterogeneity of ferroptosis susceptibility among periodontal cell subtypes, the identity of DAMPs-mediated intercellular signaling networks, and the epigenetic mechanisms governing ferroptosis-susceptibility transitions remain incompletely characterized. - Source: PubMed
Publication date: 2026/09/09
Yang HongmeiZhou Zhao - Steatotic liver grafts exhibit heightened susceptibility to hepatic ischemia-reperfusion injury (HIRI), contributing to poor outcomes in liver transplantation; however, the underling mechanisms remain incompletely defined. Here, we demonstrate that extracellular vesicles derived from steatotic livers (HFD-EVs) exacerbate HIRI by delivering acyl-CoA synthetase long-chain family member 4 (ACSL4) to hepatocytes, thereby triggering a ferroptosis-mitochondrial apoptosis cascade. Proteomic profiling revealed that HFD-EVs are enriched with ACSL4 and other pro-ferroptotic mediators, but deficient in mitochondrial oxidative phosphorylation components. In a murine model, administration of HFD-EVs to lean mice prior to ischemia-reperfusion significantly aggravated liver injury, apoptosis, and inflammatory responses compared to EVs from healthy livers. , HFD-EVs were internalized by hepatocytes, leading to ACSL4 up-regulation, GPX4 suppression, and subsequent iron-dependent lipid peroxidation. This ferroptotic stress induced mitochondrial calcium overload, permeability transition pore opening, membrane depolarization, and ultrastructural damage, culminating in cytochrome c release and apoptotic cell death. Critically, inhibition of ferroptosis with Ferrostatin-1 abolished ACSL4 induction, restored mitochondrial integrity, and rescued cell viability, confirming the central role of ferroptosis in HFD-EVs-induced injury. Our study unveils a previously unrecognized mechanism by which HFD-EVs transmit ACSL4 to initiate ferroptosis and mitochondrial dysfunction in recipient hepatocytes, providing a mechanistic basis for the vulnerability of steatotic grafts to HIRI. These findings highlight HFD-EVs and the ACSL4-ferroptosis axis as promising therapeutic targets to improve the quality of fatty liver grafts in transplantation. - Source: PubMed
Publication date: 2025/12/24
Zhao HangchengZhao JialingZhou DanfengLei YunguoLiu ZhikunChen JunHu PeiyangXu XiaoXie HaiyangWei Qiang - Immune-checkpoint inhibitors have limited activity in unselected metastatic castration-resistant prostate cancer (mCRPC), although molecularly selected subsets can respond. Androgen-receptor (AR)-linked lipid and redox remodeling creates biologically credible ferroptosis vulnerabilities, but whether ferroptosis can improve immune or radioligand therapy remains uncertain. - Source: PubMed
Publication date: 2026/09/23
Chen Chun-ChiWang Chih-JenLin Hung-Yu - Psoriasis is a complex inflammatory disease associated with keratinocyte hyperproliferation, abnormal differentiation, and hyper-inflammation. Recent advances have indicated that oxidative stress and ferroptosis contribute to the development of this pathology; however, the regulation of their mechanisms remains unclear. This research aimed to reveal the impact of lipoic acid synthase (LIAS), a mitochondrial enzyme that is critical for redox regulation, on psoriasis-like keratinocytes. LIAS expression was significantly upregulated upon stimulation of HaCaT cells with TNF-α and IL-17A at both transcriptional and translational levels. It was found that LIAS expression led to cell proliferation, migration, and pro-inflammatory cytokines production while silencing of LIAS gene inhibited these processes. Additionally, overexpression of LIAS led to an increase in intracellular ROS generation, oxidative damage, and mitochondrial dysfunction revealed by elevated mitochondrial ROS generation and reduced mitochondrial membrane potential. Moreover, LIAS influenced ferroptosis-related markers, such as GPX4, ACSL4, and FTH1. LIAS overexpression was also associated with increased activation of STAT3 and NF-κB signaling, consistent with enhanced inflammatory signaling. Moreover, LIAS inhibited keratinocyte differentiation revealed by the elevation of KRT16 expression and decreased expression of involucrin, filaggrin, and loricrin. Importantly, N-acetylcysteine and ferrostatin-1 significantly suppressed LIAS-induced effects. These results collectively identify LIAS as a regulator of psoriasis-like keratinocyte dysfunction and indicate that its effects are associated with oxidative stress, ferroptosis-related molecular remodeling, and inflammatory signaling. These findings suggest that LIAS-associated mitochondrial and redox signaling warrants further investigation in psoriasis pathogenesis. - Source: PubMed
Publication date: 2026/09/23
Zheng XiaofengXun LijuanWang LifengLiu Xiaotao - While immunotherapy has revolutionized cancer and other disease treatment, its clinical application requires effective cryopreservation for scalable manufacturing and global distribution. However, many immune cells exhibit substantial freeze-thaw sensitivity, limiting their scalable production and distribution. Using metabolic flux analysis, ROS quantification, lipidomics, and xenograft models, we identified metabolic state as a determinant of immune cell cryo-sensitivity. Natural killer (NK) cell activation induced a metabolic shift with elevated glucose utilization and excessive ROS, causing profound post-thaw viability and functional loss (∼25% survival). Targeted pretreatments-glucose metabolism inhibitors, antioxidants, and lipid peroxidation inhibitors-restored post-thaw recovery to ∼90% while preserving effector activity and antitumor efficacy in immunodeficient mice. Similar protection in αβ T cells, γδ T cells, and macrophages indicates that metabolic and oxidative features broadly emerge as key determinants of immune cell cryopreservation sensitivity. These findings support a metabolic-oxidative axis as an important feature associated with NK cell cryo-vulnerability. - Source: PubMed
Publication date: 2026/09/15
Mo ZujianYang HongweiZhang MengCao HuimeiWang LingqiTao KunChen XiaoshuaiHan CaixiaBustamante CarlosLiu ZhangWang Jianjun