Ask about this productRelated genes to: MECR Blocking Peptide
- Gene:
- MECR NIH gene
- Name:
- mitochondrial trans-2-enoyl-CoA reductase
- Previous symbol:
- -
- Synonyms:
- CGI-63, NRBF1, FASN2B, ETR1
- Chromosome:
- 1p35.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-05-24
- Date modifiied:
- 2017-02-02
Related products to: MECR Blocking Peptide
Related articles to: MECR Blocking Peptide
- 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 - Emergency triage accuracy is critical but varies with clinician experience, cognitive load, and case complexity. Mis-triage can delay care for high-risk patients and exacerbate crowding through unnecessary prioritization. Large language models (LLMs) show promise as triage decision-support tools but are vulnerable to hallucinations. Retrieval-augmented generation (RAG) may improve reliability by grounding LLM reasoning in authoritative guidelines and real clinical cases. - Source: PubMed
Publication date: 2026/01/26
Wong Hang SheungWong Tsz Kwan - Enhancing feed efficiency is central to improving both the economic viability and environmental sustainability of poultry production. Although previous research has documented how intestinal, hepatic, and muscular nutrient metabolism contributes to feed efficiency variation, less is known about corresponding differences in circulating blood. Residual feed intake (RFI) was measured in small-sized meat ducks from 21 to 42 days of age. From a natural population of 800 ducks, the eight individuals with the highest RFI and the eight with the lowest RFI were selected to form the low RFI (LRFI, RFI = -14.95) and high RFI (HRFI, RFI = 11.72) groups, respectively. Blood samples were collected at 21 days of age for plasma biochemical analysis, metabolomic profiling, and whole-blood transcriptomic analysis. Plasma biochemical analyses showed that LRFI ducks exhibited significantly reduced triglyceride (TG) concentrations and significantly elevated glucose (GLU) and creatine kinase (CK) levels relative to HRFI birds (P < 0.05). Metabolomic profiling further revealed significant suppression of the arachidonic acid and α-linolenic acid metabolic pathways in LRFI ducks (P < 0.05). Weighted gene co-expression network analysis (WGCNA) combined with protein-protein interaction analysis identified HLX, CSF1R, MECR, RICTOR, and HTT as core genes associated with RFI, based on their network connectivity, differential expression patterns between HRFI and LRFI ducks, and evidence of selection signals (P < 0.05). Integrated metabolomic-transcriptomic analyses further highlighted key blood-based indicators linked to RFI within the arachidonic acid pathway, including metabolites (PC-O, prostaglandin G2, thromboxane B2, and 5-oxo-ETE) and genes (GGT1, HPGDS, and LCN2), which may serve as early predictive markers for selecting LRFI ducks. Collectively, these results provide a systematic characterization of blood metabolic and transcriptional differences between ducks with divergent RFI and identify potential early blood-based biomarkers that may support the genetic improvement of feed efficiency in poultry. - Source: PubMed
Publication date: 2026/01/18
Zhuang ZhongLi YongpengLu YijiaBai HaoBi YulinWang ZhixiuChen ShihaoChang GuobinJiang Yong - Using medicinal plants as crude extracts for therapeutic purposes and understanding their pharmacological effects presents several difficulties. Further partitioning of crude extracts into components play crucial roles in understanding the pharmacological properties of their bioactive compounds. This study explored the biological properties of leaf, identified its bioactive compounds and molecular docking. Methanol extract of (MECR) leaf was prepared and successively partitioned into hexane (HFCR), ethyl acetate (EACR), butanol (BFCR) and aqueous (AFCR) fraction. Antioxidant, antidiabetic, and anti-inflammatory properties were performed using standard procedures. Bioactive compounds were identified using GC-MS and HPLC following molecular docking. Results revealed that MECR contained significant amounts of total phenol compared to the fractions while total flavonoid was abundant in HFCR, EACR, BFCR, and AFCR. Radicals (DPPH, ABTS and LPO) scavenging ability was above 50% across the samples while only the fractions demonstrated significant ( < ) inhibition of amylase, glucosidase and sucrase. From this study, AFCR possessed better anti-inflammatory properties compared to other samples. Chromatography analyses revealed that both extract and fractions possessed varying concentrations of bioactive compounds such as lipoidal compounds and polyphenolic compounds. Docking analyses of the most abundant phytocompound (kaempferol) revealed strong binding interactions with human amylase, SGLT-1, SGLT-2, IL-6R, and trypsin. These findings have demonstrated the pharmacological potentials (antioxidant, antidiabetic, anti-inflammatory) of the methanol extract and fractions of leaf. A potential bioactive compound from the fractions of have been identified to possess strong molecular interactions with selected protein targets. - Source: PubMed
Publication date: 2026/01/08
Akintimehin Emmanuel SinaKarigidi Kayode OlayeleFajembola Tosin FeliciaOmogunwa Tope SamuelOgunbameru Faith EstherFapetu Aanuoluwapo PatriciaAdetuyi Foluso OlutopeOnoagbe Iyere Osolase - Mitochondrial dysfunction is linked to stroke risk, but the specific genes involved remain unclear. This study aimed to identify mitochondria-related genes associated with stroke. We performed summary data-based Mendelian randomization analyses using 1136 mitochondria-related genes, integrating methylation quantitative trait loci (mQTL), expression QTL (eQTL), and protein QTL (pQTL) data with stroke-related genome-wide association study (GWAS) results. Colocalization analyses were used to assess potential shared genetic signals, followed by validation in the UK Biobank (UKB) and FinnGen cohorts. We identified 115 CpG sites, 14 genes, and 5 proteins linked to stroke. Significant colocalization was found for 26 loci, including four genes (CYC1, MECR, NGRN, NLRX1) and two proteins (LONP1, MMUT). Validation in UKB confirmed seven CpG sites, with eight confirmed in FinnGen. MMUT protein abundance was negatively associated with stroke risk (OR = 0.730). PRDX3 showed a positive methylation-expression relationship (OR = 2.733; 95% CI, 2.004-3.727), with cg01126576 methylation (OR = 0.895; 95% CI, 0.819-0.978) and expression (OR = 0.909; 95% CI, 0.838-0.986) linked to reduced stroke risk, whereas higher protein abundance was associated with increased risk (OR = 1.472; 95% CI, 1.076-2.014). PRDX3 demonstrates contrasting associations at different molecular levels, while MMUT is validated as a stroke-associated protein, highlighting both as potential priorities for future mechanistic and therapeutic studies. - Source: PubMed
Publication date: 2025/12/06
Tang XiaorongCheng GuannanChen SiyunYao LuluLu LimingShen ChenweiFeng LubaoZhang WenwenXu NengguiWang Lin