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
- This study aimed to investigate whether PM2.5 and microplastics (MPs) aggravate ovalbumin (OVA)-induced allergic airway injury and to elucidate the role of mitochondrial dysfunction-associated ferroptosis in this process. An OVA-induced murine asthma model and OVA-stimulated MRE cells were established and exposed to PM2.5 and/or MPs. Histopathological, biochemical, molecular, and functional analyses were performed to evaluate pulmonary injury, oxidative stress, ferroptosis, mitochondrial dysfunction, and inflammatory responses. In addition, OPA1 knockdown and ferrostatin-1 (Fer-1) intervention were used to verify the mechanistic involvement of ferroptosis. Exposure to PM2.5 or MPs further aggravated OVA-induced pulmonary damage, as evidenced by enhanced inflammatory infiltration, increased inflammation score, total cell counts and goblet cell percentage, and impaired lung function. In parallel, co-exposure to PM2.5 and MPs markedly intensified oxidative stress in lung tissue and MRE cells, as shown by increased ROS and MDA levels and decreased T-AOC, CAT, and SOD. Moreover, PM2.5 and MPs enhanced ferroptosis by increasing Fe accumulation, lipid peroxidation, and NCOA4, FTH1, and ACSL4 expression, while suppressing SLC7A11, GPX4, GCLC, and GSS. These effects were accompanied by profound mitochondrial dysfunction, including altered expression of mitochondria-related genes, loss of mitochondrial membrane potential, ATP depletion, reduced mitochondrial respiratory complex activities, impaired oxygen consumption rate, and decreased NADPH and GSH-related antioxidant capacity. Importantly, OPA1 silencing or Fer-1 treatment markedly attenuated PM2.5 +MPs-enhanced ferroptotic and inflammatory injury in OVA-treated MRE cells. Collectively, these findings suggest that PM2.5 and MPs co-exposure may exacerbate allergic airway injury by promoting mitochondrial dysfunction-associated ferroptosis via the OPA1/SLC7A11 pathway. - Source: PubMed
Publication date: 2026/09/16
Ma YucongLiu XidongDiao LeiZhang LuWang FangYu Xiuhua - Neuroinflammation and astrocytic ferroptosis form a self-reinforcing vicious cycle across multiple neurological disorders, constituting a core pathological mechanism driving the progression of neurodegeneration, stroke, epilepsy, autoimmune encephalopathy. Initial neuroinflammation activates microglia to release pro-inflammatory factors such as interleukin (IL)-1β and tumor necrosis factor (TNF)-α, inducing the transformation of astrocytes into a neurotoxic A1 phenotype, disrupting iron homeostasis, inhibiting the glutathione (GSH)-glutathione peroxidase 4 (GPX4) antioxidant system, activating the NADPH oxidase 4 (NOX4) and acyl-CoA synthetase long-chain family member 4 (ACSL4) pathways, and triggering ferroptosis. Damage-associated molecular patterns, [including high mobility group box 1 (HMGB1), adenosine triphosphate (ATP), and mitochondrial DNA] and pro-inflammatory mediators (including reactive oxygen species and lipid peroxidation products) released by ferroptotic cells further activate glial cells and amplify inflammation, establishing a positive feedback loop. Key regulatory nodes include forkhead box (Fox)O1a, nuclear factor (NF)-κB, nuclear factor erythroid 2-related factor 2 (Nrf2), and sirtuin 1 (SIRT1), while mitochondria-endoplasmic reticulum interactions participate in subcellular regulation. Current intervention strategies encompass iron chelation combined with antioxidants, NOX4 inhibition, blockade of A1 phenotype transformation, targeted activation of receptor tyrosine kinases, and blood-brain barrier-targeted drug delivery. However, challenges remain in cell-specific targeting, spatiotemporal dynamic monitoring, and clinical translation. Breaking this vicious cycle may offer a novel neuroprotective therapeutic direction for neurological disorders. - Source: PubMed
Publication date: 2026/08/31
Zhang LiWang DijunWang WeiqiChen JuhuaQian HongyuRuan Yonglan - Diabetes mellitus complicated with depression (T2DD) is different from a single disease. It leads to more severe damage to nerve cells and cognitive dysfunction, and has a poor prognosis. Existing evidence indicates that ferroptosis-a form of programmed cell death driven by iron accumulation and lipid peroxidation-is involved in both diabetes and depression. Glutathione peroxidase 4 (GPX4) and long-chain acyl-CoA synthetase family member 4 (ACSL4) are key regulators of ferroptosis, but their roles in T2DD-associated neural damage remain unclear. - Source: PubMed
Publication date: 2026/08/31
Wang YiWang ShuoZhao ShuaiLei YanliFan YuchengZheng XinyiYang LanMa Yanmei - Knee osteoarthritis (KOA) is a prevalent degenerative disease lacking structural disease-modifying agents. According to TCM theory, its progression involves internal liver-kidney deficiency and external qi/blood stasis with meridian obstruction. We evaluated Wangbi Capsule (WBC) plus diacerein/glucosamine vs. controls (n=180) over 12 weeks. Primary: WOMAC change; secondary: VAS, Lequesne, PhGA, HAQ. In an exploratory subgroup (n=75), PBMC mRNA for GPX4, SLC7A11, ACSL4, plus ESR, hs-CRP, and β-CTX were measured. - Source: PubMed
Publication date: 2026/09/10
Wang XiaoqingWang MeiZhao ZhenyiWen ZhongLi YanhuiLi XiuZhang Quan-BoQing Yu-Feng - Sepsis often leads to severe liver damage, and currently few effective therapies are available for it. Nicotinamide mononucleotide (NMN), a well-known anti-aging agent, exerts organ-protective effects, yet its detailed mechanisms against acute liver injury remain poorly understood. Here, we established LPS-induced liver injury mouse models, along with in vitro models using primary hepatocytes, primary macrophages and THP-1 cells. We found that LPS triggers ferroptosis and inflammation in both macrophages and hepatocytes, and paracrine inflammatory signals from macrophages further aggravate hepatocyte ferroptosis. NMN effectively reverses these pathological changes. Mechanistically, NMN suppressed mtDNA-mediated cGAS-STING activation and weakened the interaction between STING and ACSL4. Domain mapping, molecular simulations, surface plasmon resonance (SPR) analysis, co-immunoprecipitation and hepatic proximity ligation assay (PLA) collectively demonstrated that NMN destabilized the STING-ACSL4 complex, thereby restraining ferroptosis. In conclusion, NMN protects against LPS-induced acute liver injury by concurrently suppressing cGAS-STING-mediated inflammation and weakening the pro-ferroptotic STING-ACSL4 interaction. - Source: PubMed
Publication date: 2026/09/14
Liao YanZhu Cheng-LongZhang WangzheqiCheng Lin-DongLiu YangWang YiZhou TianZhao Jia-XinBian Jin-JunZou ZuiZhou Miao