Ask about this productRelated genes to: ACO2 Blocking Peptide
- Gene:
- ACO2 NIH gene
- Name:
- aconitase 2
- Previous symbol:
- -
- Synonyms:
- ACONM
- Chromosome:
- 22q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2015-12-01
Related products to: ACO2 Blocking Peptide
Related articles to: ACO2 Blocking Peptide
- Acute kidney injury (AKI) is a clinical syndrome characterized by a rapid decline in renal function, high morbidity and mortality, and a lack of effective early diagnostic markers or targeted therapies. To address this critical unmet need, we employed an integrated multi-omics and network pharmacology approach to systematically investigate the molecular mechanisms and potential therapeutic targets of AKI. Core targets were identified through differential gene expression (DEG) analysis combined with weighted gene co-expression network analysis (WGCNA), followed by exploration using protein-protein interaction (PPI) networks and pathway enrichment analyses. Inflammation, oxidative stress, and energy metabolism emerged as key pathways involved in AKI pathogenesis. Using ten CytoHubba algorithms and the MCODE module for comprehensive screening, we identified three hub genes-ACO2, FBP1, and PFKL. Their expression patterns and cellular specificity were further characterized using single-cell RNA sequencing data from AKI renal tissues. Additionally, we constructed a miRNA-hub gene regulatory network, providing insights into miRNA-based therapeutic strategies. Molecular docking analysis identified three approved drugs-Ajmaline, Cimetidine, and Tretinoin-with strong binding affinities to the hub proteins, suggesting their potential for repurposing in AKI treatment. Finally, by reviewing knockout mouse models from the Mouse Genome Informatics (MGI) database and conducting in vitro cell experiments, we explored the in vivo and in vitro roles of these core targets, providing experimental evidence of their physiological relevance. Overall, this study integrates cross-cohort transcriptomic profiling, network-based hub prioritization, single-nucleus cell-type localization, translational drug repurposing analyses, and in vitro experimental validation thereby providing a multi-layered framework to prioritize candidate biomarkers for AKI. - Source: PubMed
Publication date: 2026/05/14
Li GuoqiangZeng DianjieWang YinhuaiLiu JiachenYang Dong - Breathing disturbances during sleep are associated with intermittent hypoxaemia, arousal and sympathetic activation, which in turn lead to oxidative stress and cardiovascular and metabolic consequences. However, they are also characterised by fluctuations of carbon dioxide levels, switching between hypercapnia and hypocapnia, which contribute to acute and sustained physiological and cellular effects. Changes in arterial carbon dioxide tension ( ) influence cerebral blood flow, respiratory control and renal function. The complex pathophysiology requires the integration of clinical entities and therapeutical options based on precise measurement of CO Continuous measurements during the night best reflect nocturnal changes in CO levels. Alveolar, arterial, capillary and transcutaneous CO measurements represent distinct characterisations of CO fluctuations. Alveolar and arterial CO levels are very similar and correlate closely to the end-tidal CO ( ) in healthy subjects. However, the validity of is limited in diseases with inhomogeneous lung ventilation and, due to artefacts, during mechanical ventilation. Transcutaneous CO measurement has proven to adequately represent , although time delays in response and absolute figures can differ. Obesity hypoventilation syndrome (OHS) exemplifies a frequent clinical condition with multiple pathophysiological components impacting levels differently across 24 h. Treatment is often delayed due to limited awareness of mild hypercapnia occurring exclusively during night-time. Positive airway pressure (PAP) therapy remains the cornerstone of management. The choice between continuous positive airway pressure or noninvasive ventilation should be guided by the predominant OHS phenotype and the severity of daytime hypercapnia. Management of OHS should also focus on cardiometabolic comorbidities and include a multimodal approach to the underlying obesity. - Source: PubMed
Publication date: 2026/05/13
Randerath Winfried JFanfulla FrancescoPépin Jean Louis - Tissue hypoperfusion can persist despite meeting early goal-directed therapy targets, while excessive resuscitation poses risks. The study focuses on the utility of central venous-arterial CO2 gap to arterial-central venous O2 content difference ratio (Pv-aCO2/Ca-vO2) can serve as a valuable tool for guiding fluid resuscitation in patients with septic shock. - Source: PubMed
Fang Xue-WeiWeng Yi-RuJiang XinWu Ze-TaoYe Gong-Jie - Gastric cancer (GC) poses a significant health threat, and alterations in Fatty acid β-oxidation (FAO) may influence its progression. However, the precise mechanisms underlying this association remain unclear. FAO-related genes were analyzed using transcriptomic datasets from databases of GEO and TCGA. Totally 160 FAO-associated genes were identified, and a risk scoring model was subsequently established to stratify patients into groups of low- and high-risk. Immune characteristics, drug sensitivities, and hub genes, including IL-6, were assessed. Subsequently, immunoblotting and immunohistochemistry were performed on GC cell lines and tissue samples to evaluate IL-6 expression. Analysis of the TCGA and GEO databases revealed a FAO-related gene signature comprising ACADS, ACO2, CPT2, SLC22A5, AOC3, CD36, CIDEA, G0S2, GABARAPL1, and SERINC1. We also examined gene mutations and constructed a prognostic risk scoring model with validation achieved through a nomogram to predict gastric cancer risk. Immune infiltration analysis and drug sensitivity testing (e.g. AG-014699, Axitinib, BX-795, and Cisplatin) were also conducted. IL-6 emerged as a core gene with significant expression difference across cellular and tissue levels. FAO plays a critical role in the prognosis of GC, and IL-6 may serve as a key biomarker for diagnosis and therapeutic strategies. - Source: PubMed
Publication date: 2026/05/02
Qu ChaoYuan XuetaoYang ShutingQiao YifanZhang RenjianzhiWu YunhuaZhu MengkeDu JiayinLi GanZhang RuiSun XuejunLi Xuqi - Rice sheath blight caused by is one of the most destructive diseases of rice. Bixafen has been proposed as a promising control agent with moderate resistance risk; however, its cellular mode of action remains unclear. Therefore, this study investigated the antifungal mechanism of bixafen from the perspective of programmed cell death (PCD). Bioassays showed that bixafen strongly inhibited , with a median effective concentration (EC) of 1.16 μg/mL. Morphologically, bixafen induced hyphae collapse, vacuolization, chromatin aggregation, and mitochondrial disruption. Transcriptome analysis further revealed that bixafen significantly altered the expression of genes involved in the tricarboxylic acid cycle and PCD pathways. In addition, bixafen, at the concentration of EC, triggered ROS accumulation accompanied by increased malondialdehyde (MDA) levels. These oxidative effects led to mitochondrial damage, characterized by loss of membrane potential, reduced Tomm20 expression, and decreased Aco-2 activity. Subsequently, bixafen activated apoptosis, as evidenced by induction of the mitochondria-associated inducer of death (AMID), down-regulation of Bcl-2, and DNA fragmentation. Moreover, bixafen also induced autophagy by reducing p62 and increasing Beclin-1 expression, which suggests the clearance of damaged mitochondria. Collectively, these results demonstrated that bixafen induced mitochondrial-dependent apoptosis and autophagy in , which provided novel insights into its cellular antifungal mechanism and supported its potential as a PCD-targeted fungicide. - Source: PubMed
Publication date: 2026/03/26
Ren YuanhangHuang PingGu WentaoLi RuyiZhao YongtianLu Lidan