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
- Diabetic kidney disease (DKD) is one of the primary factors leading to end-stage renal disease. Ferroptosis, as a mechanism-related form of programmed cell death, has garnered increasing attention in DKD research. This study aimed to identify and validate ferroptosis-related diagnostic biomarkers for DKD. - Source: PubMed
Publication date: 2026/08/10
Li XuHong HuanLi HongFang ZhenhuaWang JieWang XiuliSui XintingShadekejiang HalinuerLiang MingzhuGan XinyuLiu JiamingLu Chen - This study systematically evaluated the anti-breast cancer potential and mechanisms of the cannabidiol (CBD) derivative MCPB-21. The structure of MCPB-21 was confirmed by nuclear magnetic resonance (NMR). The study analyzed differentially expressed genes associated with breast cancer using public databases and verified the binding affinity of MCPB-21 to glycogenin-2 (GYG2) through molecular docking. Additionally, the effects of MCPB-21 on apoptosis, invasion capacity, and lipid metabolism were evaluated in MDA-MB-231 and MCF-7 breast cancer cells using flow cytometry, Transwell invasion assays, cell proliferation assays, and Oil Red O staining. Western blot was employed to examine expression changes in proteins related to fatty acid β-oxidation and ferroptosis, including Acyl-CoA Oxidase 1 (ACOX1), ATP Binding Cassette Subfamily D Member 3 (ABCD3), ATP Binding Cassette Subfamily D Member 4 (ABCD4), Peroxisomal l-bifunctional enzyme (EHHADH), Carnitine palmitoyltransferase 1α (CPT1α), Glutathione Peroxidase 4 (GPX4), Solute Carrier Family 7 Member 11 (SLC7A11), and Acyl-CoA Synthetase Long Chain Family Member 4 (ACSL4). The role of fatty acid oxidation in ferroptosis was further analyzed using the ACOX1 inhibitor 10,12-Tricosadiynoic acid (500 nM). Additionally, the effects of MCPB-21 on fatty acid oxidation and ferroptosis were evaluated by interfering with GYG2 expression. Ferrostatin-1 (Fer-1) rescue experiments were conducted to verify the dependence of MCPB-21-induced cell death. Finally, the anti-tumor efficacy of various doses of MCPB-21 was compared to the control drug CBD. experimental results showed that MCPB-21 can affect the behavior of breast cancer cells by inducing cancer cell apoptosis, increasing reactive oxygen species (ROS) levels, and promoting lipid accumulation. At the same time, Western blot detection showed that MCPB-21 could downregulate key enzymes of fatty acid β-oxidation (ACOX1, ABCD3, ABCD4, EHHADH, CPT1α) and antioxidant factors (GPX4, SLC7A11), and upregulate the enzyme ACSL4 that promotes lipid peroxidation. Mechanistic studies further showed that MCPB-21 affects the expression of ACOX1 by regulating GYG2, inhibits fatty acid β-oxidation, and induces ferroptosis. At the same time, the combined use of ACOX1 inhibitors enhanced lipid accumulation and ROS levels, verifying its role in regulating fatty acid oxidation. In animal experiments, MCPB-21 (10 and 40 mg/kg) significantly inhibited the growth of nude mouse transplanted tumors, caused tumor tissue necrosis, inhibited the proliferation marker Ki67, and regulated the expression of ferroptosis-related proteins (GPX4 and SLC7A11 decreased, and ACSL4 increased). Immunohistochemical analysis showed that MCPB-21 had a stronger anti-tumor effect than CBD, mainly by regulating the fatty acid β-oxidation pathway to promote ferroptosis. In summary, MCPB-21 exhibits excellent anti-breast cancer potential. Its mechanism of action is mainly to achieve anti-tumor effects by inhibiting fatty acid β-oxidation and activating ferroptosis, which provides a theoretical basis and potential therapeutic strategy for the development of new anti-breast cancer drugs. - Source: PubMed
Publication date: 2026/07/15
Mao MengjieWang ChunyuLu YingchunTao QingxiuZeng LongLi JingLiu Bin - Perioperative neurocognitive disorder (PND) is a common complication after anesthesia and surgery, particularly in older individuals, and is associated with oxidative stress and ferroptosis. Krüppel-like factor 4 (KLF4) has been implicated in neuronal injury, but its role in PND remains unclear. Using a mouse model of sevoflurane anesthesia plus tibial fracture surgery and sevoflurane-exposed HT22 cells, we found that KLF4 was upregulated in the hippocampus after anesthesia and surgery, as well as in HT22 cells. KLF4 knockdown alleviated cognitive impairment and neuronal injury in vivo and improved cell viability while reducing apoptosis in vitro. Mechanistically, KLF4 depletion attenuated oxidative stress and ferroptosis-related changes, including reduced ROS, iron accumulation, MDA, LDH, and ACSL4 expression, together with restored GSH, antioxidant activity, GPX4, and SLC7A11 levels. Multiplex immunofluorescence showed that surgery-induced GPX4 loss and ACSL4 upregulation occurred predominantly in hippocampal neurons, whereas 4-HNE accumulation was observed in both neurons and microglia. KLF4 directly bound to the SMAD7 promoter and enhanced SMAD7 transcription. Rescue experiments showed that KLF4 overexpression reversed the protective effects of SMAD7 knockdown, and in the absence of sevoflurane, KLF4 overexpression alone induced toxicity that was only partially rescued by SMAD7 knockdown. Together, these findings suggest that KLF4 is associated with PND-related neuronal injury, potentially through SMAD7-linked oxidative stress and ferroptosis-related signaling. - Source: PubMed
Publication date: 2026/08/13
Huang ZilongLin Xuewu - Methotrexate (MTX) is a widely used chemotherapeutic and immunosuppressive agent; however, its clinical use is limited by severe testicular toxicity associated with oxidative stress, inflammation, apoptosis, and ferroptosis. Therefore, the present study investigated the protective effects of icariin-loaded nanoliposomal formulation (ICA-LNPs) against MTX-induced testicular injury in rats compared with crude icariin (ICA). Sixty adult male Sprague Dawley rats were randomly allocated into six groups: control, ICA, ICA-LNPs, MTX, MTX + ICA, and MTX + ICA-LNPs. MTX administration markedly impaired reproductive function, evidenced by significant reductions in testosterone, luteinizing hormone (LH), follicle-stimulating hormone (FSH), sperm count, motility, and viability, together with increased sperm abnormalities. MTX also disrupted the NRF2/HO-1/NQO1 signaling pathway, suppressed antioxidant defenses, and elevated oxidative stress markers. In addition, MTX significantly activated NF-κB-mediated inflammatory responses, enhanced apoptotic and ferroptotic pathways, increased iron accumulation and ACSL4 expression, and reduced GPX4 and SLC7A11 expression in testicular tissue. Histopathological examination further confirmed severe degeneration of seminiferous tubules and impaired spermatogenesis. Treatment with ICA-LNPs significantly ameliorated these alterations and demonstrated superior protective efficacy compared with crude ICA. ICA-LNPs restored reproductive hormones, improved semen quality, enhanced antioxidant status, suppressed inflammatory mediators, reduced apoptosis and ferroptosis-related markers, and preserved normal testicular histoarchitecture. Furthermore, GPX4 immunoreactivity was markedly increased, whereas ACSL4 expression was significantly reduced following ICA-LNPs treatment. In conclusion, ICA-loaded nanoliposomal formulation effectively attenuated MTX-induced testicular toxicity and was associated with reduced oxidative stress, inflammation, apoptosis, and ferroptosis, highlighting its potential as a promising therapeutic strategy for preserving male reproductive function. - Source: PubMed
Publication date: 2026/08/14
Alemam AhmedJamil SalimHassan HeshamElmorsy Ekramy M - Cardiovascular diseases (CVDs) remain the leading cause of mortality worldwide, with inflammation central to disease progression. Emerging evidence reveals intricate crosstalk between metabolic reprogramming and epigenetic modifications in cardiovascular inflammatory injury, offering novel therapeutic strategies. - Source: PubMed
Publication date: 2026/07/29
Yu XiaoyuCui CongHe JiyongGuan XiaoyuZhang Zhe