Ask about this productRelated genes to: ACSL4 Blocking Peptide
- 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 Blocking Peptide
Related articles to: ACSL4 Blocking Peptide
- Inflammatory bowel disease (IBD) is a chronic intestinal disorder characterized by excessive inflammation and intestinal damage. Known for its chronic and relapsing nature, IBD currently lacks curative pharmacological therapies. Herein, we investigated the therapeutic potential of human umbilical cord mesenchymal stem cell-derived exosomes (hucMSC-Ex) in IBD and explored the underlying mechanisms. In vivo and in vitro experiments demonstrated that the administration of hucMSC-Ex significantly attenuated inflammatory levels and ameliorated associated disease symptoms in IBD models. Concurrently, hucMSC-Ex treatment effectively modulated bile acid dysregulation in the IBD condition, contributing to the restoration of intestinal metabolic homeostasis. Mechanistically, the protective effects of hucMSC-Ex were mediated through the upregulation of farnesoid X receptor (FXR) expression. FXR, a critical regulator of intestinal homeostasis, plays a pivotal role, particularly in bile acid metabolism. Elevated FXR expression further suppressed ferroptosis in macrophages, as evidenced by reduced lipid peroxidation, diminished oxidative stress, restored iron metabolism homeostasis, and normalized expression of ferroptosis-related markers (GPX4, ACSL4, MBOAT1). Collectively, our findings indicate that hucMSC-Ex alleviates IBD by activating FXR in macrophages, thereby inhibiting lipid peroxidation and reducing ferroptosis, ultimately mitigating inflammation and ameliorating intestinal damage. This offers the potential of a FXR-targeted therapeutic strategy based on exosomes for the treatment of IBD. - Source: PubMed
Publication date: 2026/04/30
Xia YuxuanSun TingZhou MengjiaoWang BoMao Fei - Macrophage ferroptosis plays a pivotal role in sepsis-induced acute lung injury (ALI). Tangeretin (TAN), derived from the traditional Chinese medicine Chen pi (Citrus reticulata), exhibits antiproliferative, anti-invasive, anti-metastatic, and antioxidant properties. This study investigated the protective effects of TAN against sepsis-induced macrophage ferroptosis in ALI and its underlying mechanism, while also exploring whether co-delivery via extracellular vesicle (EVs) could enhance its therapeutic efficacy. - Source: PubMed
Publication date: 2026/04/28
Guo YutingHu HanrongChen YinghongWang CongweiZhang YanWang DaweiLiu Yuntao - The progression of type 2 diabetes mellitus (T2DM) is closely linked to oxidative stress-induced damage. Ferroptosis is a regulated form of cell death driven by iron-dependent lipid peroxidation. Its underlying mechanism involves an imbalance between reactive oxygen species (ROS) accumulation and cellular antioxidant defense, ultimately resulting in cell death. While puerarin has been shown to exhibit antioxidant properties, its ability to ameliorate T2DM via the ferroptosis pathway remains unclear. In this study, we combined network pharmacology, proteomics, and experimental validation to investigate the regulatory mechanisms of puerarin. Potential targets of puerarin in T2DM were identified using network pharmacology and proteomics. Oxidative stress markers-including ROS, malondialdehyde (MDA), manganese-dependent superoxide dismutase (Mn-SOD), and glutathione (GSH)-as well as insulin levels and ferroptosis-related markers such as glutathione peroxidase 4 (GPX4), cyclooxygenase-2 (COX2), and acyl-CoA synthetase long-chain family member 4 (ACSL4) were measured to assess the effect of puerarin on ferroptosis. Protein kinase B (AKT1) overexpression and knockdown models, together with nuclear factor erythroid 2-related factor 2 (NRF2) inhibitors, were used alongside Western blot analysis to investigate the pathway through which puerarin regulates ferroptosis. Results showed that palmitic acid-induced oxidative stress triggered ferroptosis in mouse pancreatic β-cells (MIN6). Under puerarin intervention, ferroptosis biomarkers including ROS, MDA, Mn-SOD, iron ions, and GSH, as well as mitochondrial morphology, were significantly altered. Mechanistic studies revealed that puerarin upregulates AKT1, leading to enhanced phosphorylation of GSK3β and increased expression of NRF2. Consequently, expression of GPX4, a key enzyme in glutathione metabolism, was elevated, thereby suppressing ferroptosis. This study is the first to identify targets of puerarin in T2DM through an integrated network pharmacology and proteomics approach. It demonstrates that puerarin may upregulate GPX4 via the AKT/GSK3β/NRF2 pathway, thereby mitigating oxidative stress damage and reducing ferroptosis, offering novel mechanistic insight for diabetes treatment. - Source: PubMed
Publication date: 2026/04/24
Chen YulinWei XiaojieLin TianLei ZiweiLi JunlinKuang HaiXu XiaohuiLiang Tao - This study aimed to investigate the effects of nicotinamide adenine dinucleotide (NAD⁺) on lung injury after cardiac arrest (CA) and cardiopulmonary resuscitation (CPR) in swine and to explore the potential underlying mechanisms. - Source: PubMed
Publication date: 2026/04/29
Chen MeisongHu YufengYang XuelinLai LinjieLiu MingjunLiu YongXu JiefengLan Pin - Neuropathic pain (NP) has become a major global public health issue. Tuina, a traditional therapy, has been shown to alleviate pain effectively by promoting nerve repair and reducing neuroinflammation. This study aimed to investigate whether Tuina can suppress the ferroptosis-autophagy pathway to improve NP induced by spinal nerve ligation (SNL) in rats. - Source: PubMed
Wang KailongYang PeipeiGan XiaofengTang HongliangTan LiangyuanHu Yueqiang