Ask about this productRelated genes to: C5AR1 Blocking Peptide
- Gene:
- C5AR1 NIH gene
- Name:
- complement C5a receptor 1
- Previous symbol:
- C5R1
- Synonyms:
- C5A, C5AR, CD88
- Chromosome:
- 19q13.32
- Locus Type:
- gene with protein product
- Date approved:
- 1991-12-04
- Date modifiied:
- 2016-08-10
Related products to: C5AR1 Blocking Peptide
Related articles to: C5AR1 Blocking Peptide
- Complement is a central effector of cell and tissue injury in hematological and autoimmune diseases, and recent intensive research brought new inhibitors to the clinic. This review summarizes complement-mediated mechanisms across hematological, systemic, and kidney-specific autoimmune diseases, appraises emerging biomarker strategies, and evaluates these therapies. - Source: PubMed
Publication date: 2026/07/28
Vasilev VasilPetkova MarianaRadanova MariaRoumenina Lubka T - Polycystic ovary syndrome (PCOS) is a heterogeneous endocrine-metabolic disorder characterized by profound disturbances in energy metabolism, yet the molecular mechanisms underlying glycolytic dysfunction remain incompletely understood. Given the essential role of glycolysis in ovarian function and endocrine homeostasis, this study aimed to systematically characterize glycolysis-associated molecular alterations in PCOS and identify key metabolic regulators involved in disease pathogenesis. Transcriptomic datasets GSE34526 and GSE6798 were integrated to identify glycolysis-related differentially expressed genes (GRDEGs). Functional enrichment, immune infiltration, and regulatory network analyzes were performed to characterize the biological features associated with glycolytic dysregulation. Machine learning algorithms, including support vector machine, random forest, logistic regression, and LASSO regression, were applied to prioritize key glycolysis-associated regulators for downstream biological characterization. The functional role of GPT2 was further examined in KGN granulosa cells under PCOS-like conditions. Twelve GRDEGs were consistently dysregulated in PCOS and were predominantly enriched in glycolytic metabolism, ATP generation, and transcriptional regulatory processes. Integrative machine learning analyzes prioritized four key glycolysis-related genes (AMPD3, C5AR1, MLXIPL, and PDLIM7) associated with glycolytic remodeling in PCOS. Immune infiltration analyzes further revealed coordinated metabolic and immune remodeling, while regulatory network analyzes highlighted extensive interactions between hub genes and miRNA-, transcription factor-, and RNA-binding protein-mediated regulatory networks. Functional experiments demonstrated that GPT2 knockdown impaired glycolytic activity, reduced ATP production and aromatase activity, disrupted steroid hormone homeostasis, and exacerbated metabolic dysfunction in granulosa cells, whereas pharmacological activation of glycolysis partially reversed these alterations. Our findings provide a comprehensive characterization of glycolytic dysregulation in PCOS and identify GPT2 as a potential metabolic regulator linking altered energy metabolism to ovarian dysfunction. These findings provide a molecular framework for future studies investigating metabolism- and nutrition-based intervention strategies in PCOS. - Source: PubMed
Publication date: 2026/09/06
Xi MeiliLuo RongkuiZhang JiarongHuang WeihongMa LiSun YunyanRen Aimin - Inflammatory bowel disease (IBD) is a chronic recurrent disorder. Gut microbiota-derived metabolites regulate intestinal homeostasis, but their molecular mechanisms in IBD remain unclear. Current studies lack systematic "microbiota-metabolite-target" network mining with multi-method validation. This study integrates network pharmacology, three machine learning algorithms, and molecular docking to construct this regulatory network in IBD. - Source: PubMed
Publication date: 2026/08/21
Hu ShanshanFu LinGao JingGuo QiongyaHan Shuangyin - Glioblastoma (GBM) is the most common and lethal primary malignant brain tumor in adults, with a median survival of approximately 15 months despite maximal multimodal therapy. The complement system plays a paradoxical dual role in GBM, mediating both antitumor immunity and immunosuppressive signaling within the tumor microenvironment, yet no systematic synthesis of complement-targeted therapeutic strategies exists. We aimed to comprehensively identify, appraise, and synthesize studies investigating complement-targeted therapies and complement-associated prognosis in GBM. Following PRISMA 2020 guidelines, we searched PubMed/MEDLINE and the Cochrane Library (CENTRAL) without date or language restrictions. Preclinical and clinical study designs were eligible. Risk of bias was assessed using SYRCLE, ROBINS-I, and study-type-specific checklists. Certainty of evidence was evaluated using GRADE. Statistical pooling was planned only for sufficiently comparable studies; clinical prognostic studies were synthesized narratively because they assessed non-equivalent constructs. Forty-one studies were included, comprising 15 preclinical in vivo, 13 preclinical in vitro, 6 clinical observational, and 7 bioinformatics studies. Five preclinical survival studies entered a structured quantitative synthesis, but no pooled cross-target effect was calculated because their interventions, comparators, and reported summary measures were non-equivalent. Clinical prognostic studies evaluated either individual protein biomarkers or multigene immune-risk signatures and were not pooled. GRADE certainty was "Very Low" for both outcomes. C3b opsonization and the C5a/C5aR1 axis were among the most frequently studied targets. Complement modulation remains a promising biological hypothesis in GBM rather than evidence for clinical application, and certainty of evidence is very low. Methodological and mechanistic heterogeneity across complement targets underscore the need for standardized preclinical models and randomized clinical trials. - Source: PubMed
Publication date: 2026/07/29
Walton Chase MStrickland Ben A - Microglial pro-inflammatory activation contributes to neuroinflammatory processes in many neurological disorders. Saturated fatty acids such as palmitic acid (PA) are increasingly recognized as inflammatory cues, yet the molecular mechanisms linking PA to microglial inflammatory responses remain incompletely defined. In this study, using BV-2 microglia as an exploratory in vitro model, we investigated whether C5aR1-sensitive signaling and JMJD3/H3K27me3-related epigenetic changes are involved in PA-associated inflammatory responses. PA exposure increased Iba1 expression, altered CD86/CD206 expression, and enhanced the secretion of IL-1β, IL-6 and TNF-α. Exogenous C5a produced broadly similar inflammatory changes. Under heat-inactivated serum conditions, PA increased cell-associated C5a immunoreactivity and extracellular C5a levels, and these C5a-related readouts were reduced by PMX53. PMX53 also attenuated PA-associated increases in inflammatory markers and in the expression of TLR4, total NF-κB p65, c-Fos, and c-Jun. In parallel, PA and C5a increased JMJD3 expression and JMJD3 enrichment at selected IL-1β and IL-6 promoter regions, accompanied by reduced H3K27me3 enrichment at these loci. Pharmacological KDM6 inhibition with GSK-J4 attenuated PA-associated increases in IL-1β and IL-6 expression. Together, these findings support the involvement of C5aR1-sensitive inflammatory signaling and JMJD3/H3K27me3-related epigenetic regulation in PA-associated microglial inflammatory responses. - Source: PubMed
Publication date: 2026/08/26
Chen LiqingXu SanqingLiu YanLuo Xiaoping