Ask about this productRelated genes to: OXSM Blocking Peptide
- Gene:
- OXSM NIH gene
- Name:
- 3-oxoacyl-ACP synthase, mitochondrial
- Previous symbol:
- -
- Synonyms:
- KS, FLJ20604, FASN2D, CEM1
- Chromosome:
- 3p24.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-12-21
- Date modifiied:
- 2019-02-26
Related products to: OXSM Blocking Peptide
Related articles to: OXSM Blocking Peptide
- Particulate matter 2.5 (PM2.5) is a major environmental pollutant linked to neurological disorders through poorly understood mechanisms. We investigated whether PM2.5 induces disulfidptosis, a novel form of regulated cell death characterized by NADPH depletion and disulfide stress, in neuronal cells. Combining bioinformatics analysis of a PM2.5-exposed human cohort (GSE60767, n = 466) with in vitro experiments in primary neurons and in vivo validation in rats, we identified a characteristic molecular signature featuring SLC3A2 upregulation and OXSM downregulation (p < 0.01). This imbalance was associated with significant immune dysregulation (elevated memory B cells, CD8 T cells, and Tregs; reduced monocytes) and metabolic disturbances (NADP+/NADPH imbalance, cystine overload). Direct evidence from non-reducing Western blot confirmed disulfide-mediated actin crosslinking in both cultured neurons and hippocampal tissues of PM2.5-exposed rats. Lentiviral manipulation revealed a unidirectional regulatory relationship wherein SLC3A2 knockdown (RNAi-SLC3A2) increased OXSM expression, while OXSM overexpression (OE-OXSM) did not affect SLC3A2 levels. Both RNAi-SLC3A2 and OE-OXSM interventions improved neuronal survival and normalized NADP+/NADPH ratios after PM2.5 exposure (200 μg/mL). However, RNAi-SLC3A2 significantly inhibited cystine uptake. Correspondingly, RNAi-SLC3A2 demonstrated more robust neuroprotection compared to OE-OXSM, as evidenced by greater improvements in neuronal viability and complete restoration of action potential amplitude. Collectively, these findings establish that PM2.5 induces neuronal disulfidptosis through hierarchical SLC3A2-OXSM axis dysregulation and identify this unidirectional relationship as a novel therapeutic target for PM2.5-associated neurological injury. - Source: PubMed
Publication date: 2026/05/07
He LinaLi DongmeiWei XingWang XiaojuanCao YingyingZhou MuhuaHe KunmeiHe JunruiLuo Xibao - Ewing's sarcoma (ES) is a malignant osseous neoplasm characterized by a dismal prognosis, particularly in its metastatic variant. The significance of disulfidptosis-a newly identified cell death mechanism induced by cystine metabolic imbalance and mitochondrial dysfunction-has yet to be investigated in ES. Thus, the aim of this study was to assess the prognostic significance of disulfidptosis-related genes (DRGs) in this disease. - Source: PubMed
Publication date: 2026/04/15
Wang ZhenyangChen YongqinYang YuxuanQi LeiXu BitengLi KeWang LiangJiao Xiejia - Colon cancer (CC), characterized by high incidence and mortality, ranks among the most prevalent digestive malignancies, and reliable molecular tools to predict prognosis and immunotherapy response are needed. Disulfidptosis is a recently identified form of programmed cell death induced by disulfide stress and represents a potential therapeutic target for CC. However, the prognostic and immunological implications of disulfidptosis-related genes (DRGs) in CC remain underexplored. - Source: PubMed
Publication date: 2026/01/28
Jiang WeiYang HuaxiaLi RuiLi YanzhiXia Shaoyou - Diabetic foot ulcer (DFU) is one of the most common and severe complications of diabetes, with vascular changes, neuropathy, and infections being the primary pathological mechanisms. Disulfidptosis, a recently identified form of programmed cell death, might be involved in the development of diabetic complications. This study aims to identify and validate potential disulfidptosis biomarkers associated with DFU through bioinformatics and machine learning analysis. - Source: PubMed
Publication date: 2025/10/08
Li JIeShi HongshuoCao Yemin - Hypertension is a cardiovascular disorder characterized by sustained elevation of arterial blood pressure, in which vascular dysfunction serves as a key initiating factor leading to target organ injury. The indole alkaloid edulinine (Edu) represents a potential therapeutic agent for hypertension, although its specific mechanisms remain unclear. This study investigated the protective effects of Edu on vascular endothelial injury in N-nitro-L-arginine-induced hypertensive rats using physiological, biochemical, and histopathological assessments. Through integrated proteomic and metabolomic analyses, we examined Edu's effects on thoracic aortic tissue proteins and serum metabolic profiles to elucidate its molecular mechanisms. The results demonstrated that Edu exhibited superior antihypertensive efficacy compared to sodium nitroprusside and effectively ameliorated hypertension-induced left ventricular systolic dysfunction. Furthermore, proteomic analysis indicated that compared with the Model group, Edu showed significant intersections in the tricarboxylic acid cycle, fatty acid degradation, oxidative phosphorylation, and fatty acid elongation pathways. These pathways are of great significance to lipid metabolism and energy metabolism and are closely related to fatty acid elongation and myocardial contraction. In the fatty acid degradation pathway, the proteins up-regulated by Edu almost exactly correspond to those down-regulated by the Control group. Metabolomics analysis revealed that Edu exerts its antihypertensive effects primarily by regulating biological pathways involved in bile acid metabolism, fatty acid metabolism, and lipid metabolism. The integrated analysis of metabolomics and proteomics demonstrated that Edu markedly reduced the abnormal up-regulation of OXSM and MECR in hypertensive rats, suggesting that Edu may systematically regulate the balance of the fatty acid metabolic network by regulating the carbon chain initiation and elongation processes in fatty acid synthesis, as well as the key reductive reactions in mitochondrial β-oxidation. In summary, the potential mechanism of the protective effect and antihypertensive effect of Edu on the thoracic aorta of L-NNA-induced hypertensive rats may be inhibiting the up-regulation of OXSM and MECR expression, regulating the dynamic balance of fatty acid degradation and synthesis, and improving fatty acid metabolism disorders. These findings indicate that Edu holds substantial research value as a potential therapeutic candidate for hypertension. - Source: PubMed
Publication date: 2025/11/26
Tao LingJian JunyouChen TingtingWu XingjieJiang FeiMing HuaijuHan DayaoZhang GuangqiongLi LingyanLiu ShaoboYuan ChunmaoShen XiangchunHao Xiaojiang