Ask about this productRelated genes to: SAA1 protein
- Gene:
- SAA1 NIH gene
- Name:
- serum amyloid A1
- Previous symbol:
- SAA
- Synonyms:
- PIG4, TP53I4
- Chromosome:
- 11p15.1
- Locus Type:
- gene with protein product
- Date approved:
- 1988-01-18
- Date modifiied:
- 2015-09-09
Related products to: SAA1 protein
Related articles to: SAA1 protein
- Innate immune molecules like CRP and SAA are established biomarkers in bacterial pneumonia, but their role in viral CAP is rarely investigated. - Source: PubMed
Publication date: 2026/09/22
Liang LifangHuang LinnaWang YiminXu JiuyangHuang YijiaoCao HongyunYuan YingyingWang WeiyangHe YanhuaQiu LijieZhan QingyuanWang ZaiCao Bin - Understanding systemic determinants of breast tumor immunity requires bridging transcriptomically distinct tissue compartments that cannot be sampled simultaneously in a single patient. We developed an MMD-regularized Domain Adaptation Autoencoder (DAA) to align unpaired RNA-seq profiles from GTEx neuroendocrine tissues (n=189) and TCGA-BRCA tumors (n=1391) within a shared 128-dimensional latent space, enabling the first cross-tissue transcriptomic interrogation of the neuroendocrine-breast tumor immune interface. The dominant cross-tissue axis was identified by Pearson correlation and rigorously validated by permutation testing (n=1000 iterations), then independently assessed in METABRIC microarray (n=1980) and SCAN-B RNA-seq (n=3273) cohorts via a strict gene-intersection protocol that eliminated zero-padding artefacts. The DAA achieved stable cross-domain alignment (mixing score =26.58%), and Latent Dimension 31 emerged as a significant systemic immune-inflammatory axis (p=0.001; aggregate correlation 13.9× above the permutation null), driven by T-cell receptor variable chains, immunoglobulin genes, and the tolerogenic phospholipase PLA2G2D. METABRIC validation recovered a mechanistically concordant acute-phase secretory signature (LBP, SAA1, PLA2G2A), while SCAN-B confirmed PLA2G2D and CCL18 on a unified cross-platform latent axis. The latent score significantly stratified overall survival (p=0.0036) and relapse-free survival (p=0.0084), and precisely reproduced the established breast cancer immune topology across all six molecular subtypes (Kruskal-Wallis H=139.4, p<0.0001). External validation in the independent neoadjuvant GEO cohort GSE25066 (n=508; Affymetrix GPL96) via a Strict Intersection Protocol (604-gene intersection, zero-padding eliminated) confirmed axis recovery (Latent Dimension 115; PLA2G2D |r|=0.266), significant distant relapse-free survival stratification (log-rank p=0.022), and non-significant pathological complete response to chemotherapy (p=0.241), establishing the axis as a prognostic but not predictive biomarker. Functional annotation in GSE25066 revealed significant correlation with all 12 curated immune cell signatures (Spearman ρ=0.10-0.42; all p<0.05), and GSEA pre-ranked analysis across 13,236 genes identified 34 significantly enriched Hallmark pathways (FDR < 0.25), led by Interferon Gamma Response (NES =2.90) and opposed by Estrogen Response Early (NES =-2.71). These findings, validated across 7152 patients in four independent cohorts, provide a computational transcriptomic framework linking systemic neuroendocrine regulation to breast tumor immunobiology and nominate PLA2G2D, SAA1, and LBP as candidate circulating biomarkers warranting prospective proteomic validation. - Source: PubMed
Publication date: 2026/09/19
Nabil HezilBouridane AhmedAl-Maadeed SomayaTalaat ImanHamoudi Rifat - Adipose tissue, once considered a passive fuel store, is now recognized as a dynamic endocrine organ that shapes cancer behavior. Within the tumor microenvironment (TME), cancer-associated adipocytes (CAAs) undergo marked reprogramming-losing large lipid droplets, adopting fibroblast-like features, and intensifying lipolysis-while releasing proinflammatory mediators that accelerate proliferation, invasion, and therapy resistance. This interaction is bidirectional: through cytokines, adipokines, and extracellular vesicles (including exosomal microRNAs), CAAs coordinate immune recruitment, extracellular matrix (ECM) remodeling, and angiogenesis. Mechanistically, several pathways converge at this interface. YAP/TAZ, STAT3, and PI3K/AKT integrate mechanical stress, inflammatory tone, and nutrient cues; metabolic symbiosis-enhanced fatty acid oxidation alongside glycolytic rewiring-supplies energy and redox support. CAAs also amplify metastasis and chemoresistance, particularly in triple-negative breast (TNBC) and pancreatic cancers, via effectors such as CXCL8, FAM3C, and SAA1. Systemic axes also matter in cancer cachexia, adipocyte-derived lipocalin-2 (LCN2) promotes tissue wasting and dampens thermogenesis, while obesity's chronic inflammation further biases the TME toward tumor promotion. This review synthesizes how CAAs and adipose dynamics drive oncogenesis, progression and therapeutic failure and highlights actionable nodes within the adipose-tumor axis for precision oncology. - Source: PubMed
Publication date: 2026/08/25
Shi JinminAbdel-Ghany ShaimaaAbdel-Fattah MariamHu XueboWadan Al-Hassan SolimanSabit Hussein - Hypertensive disorders of pregnancy (HDP) confer increased cardiovascular disease (CVD) risk postpartum. Screening methods targeting women with increased risk are lacking, limiting personalized follow-up. Circulating biomarkers may assist CVD risk stratification. We aimed to assess whether circulating biomarkers were associated with measures of cardiovascular structure and function following HDP and normotensive pregnancies (controls). We examined 275 women 1-3 years postpartum (176 following HDP and 99 parous controls). Circulating biomarkers (hs-CRP, non-HDL cholesterol, glucose, eGFR, cTnT, NT-proBNP, GDF-15, sHLA-G, SAA1) and cardiovascular function and structure measures were examined [pulse wave velocity (PWV), carotid intima-media thickness (CIMT) and echocardiography]. Group differences were tested by Mann-Whitney U test and chi-square. Associations were assessed by univariate regression analyses. A p-value < 0.05 was considered statistically significant. Women following HDP displayed significantly higher rates of hypertension (5% vs. 0%) and metabolic syndrome (7% vs. 1%) than controls. Circulating biomarker levels were similar between study groups. In univariate regression analyses for the prior HDP group, non-HDL cholesterol was significantly associated with PWV and CIMT. Additionally, glucose and hs-CRP were significantly associated with PWV. These associations were not reproduced for controls, except for non-HDL cholesterol which was significantly associated with CIMT. In conclusion, women following HDP and normotensive pregnancies had similar postpartum levels of circulating biomarkers, but circulating biomarkers were significantly associated with measures of arterial stiffness (PWV and CIMT) in women with prior HDP. Our findings support current guidelines recommending CVD follow-up after HDP. Non-HDL cholesterol, glucose and hs-CRP may possibly help refining personalized cardiovascular follow-up postpartum. - Source: PubMed
Publication date: 2026/08/21
Klepp KristinaMoe KjartanJacobsen Daniel PSugulle MeryamAngel Kristinvon Lueder Thomas GDechend RalfStaff Anne Cathrine - Brain-heart syndrome (BHS) describes cardiac dysfunction secondary to central nervous system injury, with acute ischemic stroke (AIS) serving as a critical driver that exacerbates myocardial infarction (MI). This study aimed to elucidate the role of Apolipoprotein M (APOM) in stroke-aggravated MI and to explore its underlying systemic and molecular mechanisms. Clinical data were analyzed to evaluate the correlation between stroke and MI. A combined mouse model of middle cerebral artery occlusion (MCAO) and MI was established to assess neurological and cardiac injury. Quantitative proteomics and Weighted Gene Co-expression Network Analysis (WGCNA) were employed to screen key differentially expressed proteins. The role of APOM in myocardial injury was validated using APOM-knockout (KO) mice. Furthermore, nuclear-cytoplasmic fractionation, immunofluorescence, and Western blot were performed to investigate its effects on the Saa1 and NF-κB signaling, NLRP3-related inflammatory signaling pathway, and lipid metabolism pathways. Clinical analysis indicated that stroke is a significant risk factor for MI (OR = 4.5). In the mouse model, MCAO significantly exacerbated post-MI electrocardiographic abnormalities, myocardial inflammatory response, while elevating circulating levels of cTnT and IL-1β. Proteomics identified a significant downregulation of APOM in the heart, brain, and serum post-stroke, a trend consistent with observations in AIS patients. Further experiments revealed that APOM deficiency markedly worsened cardiac conduction disturbances, histological damage, and inflammatory responses in MI mice. Mechanistically, the loss of APOM upregulates the acute-phase protein Saa1, triggers NF-κB phosphorylation and nuclear translocation, and enhances inflammatory signaling related to inflammasomes, while simultaneously mediating cytokine release from cardiomyocytes. Concurrently, APOM deficiency led to a significant decrease in sphingosine-1-phosphate (S1P) and also caused myocardial lipid droplet accumulation and metabolite changes. Additionally, the loss of APOM increased the expression of D-dimer and fibrinogen family proteins. Our findings suggest that APOM is a potential cardioprotective agent post-AIS. Downregulation of APOM may exacerbate myocardial injury after MI by elevating Saa1 expression, activating the NF-κB pathway and the inflammasome-mediated signaling, and inducing lipid metabolic disorders and coagulation-associated alterations. APOM may represent a potential therapeutic target for the intervention of brain-heart syndrome. - Source: PubMed
Publication date: 2026/08/20
Wang MinDi DongmeiQian YongxiangWang BinZhang Xiaoying