HMGCR Antibody
- Known as:
- HMGCR Antibody
- Catalog number:
- csb-pa010565la01hu
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- CusAb
- Gene target:
- HMGCR Antibody
Related genes to: HMGCR Antibody
- Gene:
- HMGCR NIH gene
- Name:
- 3-hydroxy-3-methylglutaryl-CoA reductase
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 5q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-10-05
Related products to: HMGCR Antibody
Related articles to: HMGCR Antibody
- Prostate cancer (PCa) is one of the most prevalent malignancies in men worldwide, and metabolic reprogramming particularly of lipid metabolism plays a pivotal role in its initiation and progression. Lipid biosynthesis and cholesterol regulation are closely linked to androgen receptor signaling and therapeutic resistance. However, the molecular mechanisms underlying lipid metabolic heterogeneity in prostate cancer remain poorly understood. We integrated multi-omics, single-cell RNA sequencing (scRNA-seq), and spatial transcriptomic data to characterize lipid metabolism-related gene expression in prostate cancer. Public datasets, including TCGA-PRAD and GSE206962, were analyzed using R-based bioinformatics pipelines. Machine learning algorithms, including LASSO-Cox regression and regularized Cox modeling, were applied to identify prognostic lipid metabolism-associated hub genes. Functional enrichment, pseudotime trajectory, and pathway analyses were performed to explore lipid metabolic reprogramming and its association with clinical outcomes. Single-cell transcriptomic analysis revealed marked heterogeneity in lipid metabolic activity across prostate cancer cell populations, with epithelial and endothelial clusters exhibiting the highest metabolic scores. Key hub genes HMGCR, MVK, STARD3, FADS1, and APOE were identified as central regulators of fatty acid and cholesterol metabolism. Spatial transcriptomic mapping showed region-specific enrichment of fatty acid biosynthesis and β-oxidation pathways within tumor tissue. From this module, five genes demonstrated independent prognostic value in the multivariate LASSO-Cox analysis and were subsequently used to construct the optimized prognostic signature. Thus, the 5-gene WGCNA-derived lipid metabolism module panel represents the full pool of biologically relevant candidates, whereas the 5-gene subset constitutes the final risk model. This integrative analysis demonstrates that lipid metabolism reprogramming is a major driver of prostate cancer progression and therapeutic resistance. Machine learning and single-cell approaches revealed key lipid metabolism-related biomarkers with strong prognostic potential. Targeting lipid biosynthesis and cholesterol pathways may provide new opportunities for personalized therapy and improved disease management in prostate cancer. - Source: PubMed
Publication date: 2026/06/26
Hashemi Karoii DanialQorbanee AliAzizi HosseinSamadi FatemehBehrouzkoulaei NiloufarSkutella Thomas - Oncogenic viruses, which are causative for some cancers, are typically acquired in youth and suppressed until older age. These malignancies account for over 10% of the cancer burden and often reprogram cellular metabolic pathways to promote their own survival and proliferation, often targeting lipogenic pathways to increase bioavailability of cellular products. The isoprenoid biosynthesis pathway (IBP) is an important lipogenic pathway that has been explored extensively for its dysregulation contributing to carcinogenesis, with notable discussion of statin therapy as a means of perturbing neoplasia. To our knowledge, we are the first group to provide a comprehensive discussion of the seven known oncogenic viruses and their reliance upon the IBP to promote tumorigenesis. As knowledge on this topic is limited, we aim to draw attention to a neglected area of the oncogenic research space, while also highlighting the use of inhibitors of the IBP as potential avenues for novel treatment options. - Source: PubMed
Publication date: 2026/05/31
Blaha Louise NNeighbors Jeffrey DSandeep RichaKondaka AkhilaHohl Raymond J - : Muscle symptoms are the most visible adverse event attributed to statins, but terminology is often imprecise. Most patients report myalgia or nonspecific aches, whereas objective myopathy, inflammatory or necrotizing myositis, rhabdomyolysis, and anti-HMGCR immune-mediated necrotizing myopathy are uncommon and clinically distinct entities. To provide a clinically oriented narrative synthesis of statin-associated muscle symptoms (SAMS) and severe statin-associated myotoxicity, and to propose a practical prevention, evaluation, and management algorithm. The classification of muscle events is used to standardize terminology and avoid diagnostic confusion, not to create a new formal taxonomy. : A clinically oriented narrative review was performed using PubMed, Google Scholar, and major society documents published from January 2021 to April 2026. Eligible sources addressed SAMS, statin myopathy/myositis, rhabdomyolysis, anti-HMGCR immune-mediated necrotizing myopathy, nocebo/drucebo effects, pharmacogenetics, drug interactions, diagnosis, or management. The final evidence set comprised 55 verifiable sources, including blinded randomized or n-of-1/crossover evidence; meta-analyses; clinical statements and reviews; pharmacovigilance analyses; pharmacogenetic guidance; mechanism-focused reviews; anti-HMGCR series; and lipid-lowering guideline/treatment studies. Because the review was narrative, no pooled estimate or formal PRISMA screening log was generated. : Blinded evidence indicates only a small absolute excess of muscle pain with statins, concentrated mainly in the first year of therapy, and that most muscle symptoms reported during statin therapy are not pharmacologically caused by the statin. N-of-1 and crossover trials show that symptom intensity is often similar during statin and placebo periods, consistent with an important nocebo/drucebo contribution. Severe muscle toxicity can nevertheless occur, especially when systemic statin exposure is increased by a high dose, interacting drugs, frailty, renal or hepatic impairment, hypothyroidism, transporter or metabolic genotypes, or intense unaccustomed exercise. Statin choice matters chiefly through dose, pharmacokinetics, and interaction burden. : SAMS are common as reported clinical problems, but confirmed statin-caused muscle injury is substantially less frequent than routine clinical attribution suggests. Permanent discontinuation should be reserved for carefully assessed cases. A structured approach-baseline risk assessment, selective CK measurement, exclusion of alternative causes, correction of modifiable risks, dechallenge/rechallenge, statin switching, dose reduction, and combination with non-statin therapy-preserves cardiovascular benefit while protecting the rare patient with genuine toxicity. - Source: PubMed
Publication date: 2026/06/10
Epelde Francisco - Modulation of cholesterol metabolism and reduction in serum cholesterol are key strategies for preventing cardiovascular diseases (CVDs). Functional foods enriched with dietary fiber and phytochemicals have attracted increasing attention for their potential health benefits. In this study, milk tablets containing kale and carrot (KC) were developed and preliminarily evaluated for their cholesterol-lowering potential. KC milk tablets were rich in dietary fiber, contained gallic acid, and exhibited antioxidant properties. They also supported the growth of and , accompanied by increased SCFA production. In an open-label, pre-post exploratory study in hypercholesterolemic subjects, daily consumption for 6 weeks was associated with significantly increased HDL-C and reduced LDL-C levels. In addition, circulating ApoB100 and HMGCR levels were reduced, whereas ApoE and TNF-α remained unchanged. Therefore, these preliminary findings suggest that KC milk tablets may accomplish beneficial changes in lipid profiles and support the potential of dietary fiber-phenolic interactions with enhanced SCFA production which might modulate cholesterol metabolism. However, in further studies, randomized controlled trials are required to understand the precise underlying mechanism. - Source: PubMed
Publication date: 2026/06/21
Palachai NutPolyiam PontapanDissook SivamokeKo-Iam WasanaYingthongchai PratoompornWang HechenKhongrum Jurairat - Central chondrosarcoma is the second most common primary malignant bone tumour, and grade progression markedly worsens prognosis. The contributions of lipid metabolic reprogramming and epigenetic co-dysregulation to grade progression remain poorly characterised. We integrated a bulk RNA-seq discovery cohort of 53 graded central chondrosarcomas (GSE299759) with a single-cell analysis of eight chondrosarcomas (GSE184118). Because the atypical cartilaginous tumour (ACT) and dedifferentiated groups each comprised only three samples, the Grade 3 versus Grade 2 contrast was pre-specified as the primary comparison. Curated panels of 44 lipid metabolism genes and 50 epigenetic regulators were assessed by differential expression and a correlation-based connectivity ranking, evaluated by permutation testing. In the primary Grade 3 versus Grade 2 comparison, , , and were upregulated (FDR < 0.05), indicating a grade-associated increase in de novo lipogenesis. In the exploratory Grade 3 versus ACT comparison, additional lipid genes (, ) and the epigenetic regulators and showed altered expression, although the small ACT group limits these estimates. A connectivity ranking highlighted , , , , and ; permutation testing confirmed this co-expression structure was non-random ( < 0.0001). Single-cell analysis showed , , and are expressed predominantly in malignant cells, whereas and are not, indicating cell-type heterogeneity. De novo lipogenesis upregulation is the most consistent lipid alteration in high-grade central chondrosarcoma, nominating , , and as candidates for experimental investigation. - Source: PubMed
Publication date: 2026/06/11
Ayhan BatuhanDönmez NeslihanAyhan Zeliha Deniz