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
- Postmenopausal osteoporosis (PMOP) is characterized by exacerbated bone resorption and inadequate bone formation, with macrophage-driven inflammation playing a key role. However, how immunometabolic reprogramming of macrophages modulates osteoblast fate remains unknown. - Source: PubMed
Publication date: 2026/05/03
Gu YifanWang KunWang YicongWang ZiruLi YihengLi LeiJiang ShuaiZheng YuFeng RunYang Min - Bisphenol A (BPA), is a xenoestrogen used in plastic manufacturing companies. Some countries are limiting the use of BPA. The widespread use of BPA has resulted in its accumulation in the natural environment. This compound is extensively utilised in various industrial products and is linked to harmful effects on both wildlife and human health. In recent years, extensive research has focused on ferroptosis-an iron-dependent form of programmed cell death characterised by lipid peroxidation. Also, several studies highlight the involvement of ferroptosis in mediating the toxic effects of environmental pollutants. This study aimed to deepen our understanding of BPA-induced ferroptosis by investing its impact on the antioxidant defence system, the structural integrity (as indicated by the rate of haemolysis), and the functionality of red blood cells. The research focused on evaluating the toxic effects of BPA through biochemical and haematological analyses conducted on RBCs of rats. To evaluate the involvement of ferroptotic cell death in BPA-induced toxicity, ferroptosis inducer RSL-3 and ferroptosis inhibitor Ferrostatin were used in the study either alone or in co-administration with highest concentration of BPA. The results showed that compared to the vehicle treated control group, after acute exposure of RBCs to BPA showed a notable decrease in Hb (haemoglobin) content and number of red blood cells. The ferroptotic markers viz. lipid peroxidation, GPx4 levels and ACSL4 activity were observed across all treatment groups. The results showed the possible involvement of ferroptosis on all these markers which were confirmed in the presence of ferroptosis inducer and inhibitor. Also, oxidative and nitrosative stress levels increased in a concentration-dependent manner of BPA. Furthermore, the activity of two important antioxidant enzymes; superoxide dismutase, and catalase lowered notably after BPA treatment. Results also showed significant morphological alterations, and increased membrane damage of RBC upon of BPA treatment. The study concludes that BPA exhibits oxidative stress, which may be one of the mechanisms causing RBC toxicity. The present study indicated that ferroptosis plays a key role in the progression of BPA-induced RBC toxicity; thus it can become a novel target in treatment of haemolysis. - Source: PubMed
Naga Vaishnavi MSrivastava NidhiSharma Ankita - Energy stress-induced dysfunction of granulosa cells (GCs) is a major etiological factor in diminished female reproductive performance. Although vitamin E affords cytoprotection to GCs, its specific mechanisms of action under energy stress conditions in the yak model remain unclear. - Source: PubMed
Publication date: 2026/05/02
Zhang HechengYe GuorongBai LinjiaoDu PeiyanWang MengjiaoFeng FurongLi HongliangMa XueliLu JiameiFan Jiangfeng - Ferroptosis-a regulated, iron-dependent cell death driven by lipid peroxidation-has been implicated in vascular pathology, yet how endoplasmic reticulum (ER) stress couples to ferroptotic execution in vascular smooth muscle cells (VSMCs) remains unclear. We investigated whether the PERK-EIF2α-ATF4-CHAC1 signalling axis links ER stress to ferroptosis in human aortic SMCs. Human aortic smooth muscle cells (HASMCs) and primary aortic smooth muscle cells (AoSMCs) were exposed to erastin (± ferrostatin-1), with pharmacologic modulation using buthionine sulfoximine (BSO; glutamate-cysteine ligase inhibitor) and salubrinal (selective EIF2α dephosphorylation inhibitor). Viability (CCK-8), ER-stress markers (p-PERK, p-EIF2α, GRP78, ATF4, CHAC1) and ferroptosis effectors (GPX4, ACSL4, ALOX15) were quantified by Western blotting and densitometry. Immunofluorescence assessed GPX4 and p-EIF2α/CHAC1 colocalization. Lipid peroxidation was evaluated by C11-BODIPY 581/591 imaging and malondialdehyde (MDA) content; labile Fe was measured by calcein-AM quenching; apoptosis was examined by TUNEL. Statistics used t-tests or one-way ANOVA. Erastin reduced viability and activated the EIF2α-ATF4-CHAC1 pathway in both HASMCs and AoSMCs, as evidenced by increased p-EIF2α/ATF4/CHAC1 and decreased GPX4, with concomitant upregulation of ACSL4 and ALOX15. GPX4 immunofluorescence declined, while C11-BODIPY and MDA indicated robust lipid peroxidation, and calcein-AM revealed expansion of the labile Fe pool; ferrostatin-1 mitigated these changes. BSO further amplified p-PERK→p-EIF2α → ATF4 → CHAC1 signalling and deepened GPX4 loss, whereas salubrinal sustained EIF2α phosphorylation, augmented ATF4/CHAC1, and further depressed GPX4. Across conditions, effects were consistent in both cell types and reached statistical significance (most p < 0.05 to < 0.01). ER-stress signalling via PERK-EIF2α-ATF4-CHAC1 constitutes a proximal driver of ferroptosis in human aortic SMCs by eroding glutathione tone and disabling GPX4, thereby promoting lipid peroxidation in an iron-rich milieu. Pharmacologic tuning of EIF2α phosphorylation and glutathione biosynthesis modulates ferroptotic susceptibility, nominating EIF2α-ATF4-CHAC1, GPX4/GSH homeostasis and iron handling as actionable nodes to preserve VSMC integrity in oxidizing vascular environments. - Source: PubMed
Fang ChangwenDu XiaolongWang YadanJin YiqiWang Wenbin - Ovarian cancer poses the greatest threat to survival among gynecologic cancers in women. Long non-coding RNAs (lncRNAs) have emerged as critical regulators in oncogenesis. The current study aimed to elucidate the function and regulatory mechanism of lncRNA KRT7-AS in ovarian cancer. - Source: PubMed
Publication date: 2026/04/22
Zhu YanGuan BinGuan WencaiZhang JihongWang ShiyuShi JiminFan WeiLu QiZhang LingyunXu Guoxiong