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
- 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 - Clear cell renal cell carcinoma (ccRCC) is the most common kidney malignancy. Yet, no rapid, non-invasive biomarkers are available for diagnosis or screening. Urine represents an ideal analyte matrix due to its accessibility, low invasiveness, longitudinal sampling, and the kidney's central role in filtration. Here, we integrated proteomic, lipidomic, and metabolomic analyses of urine from ccRCC patients and controls to identify diagnostic biomarkers. Multi-omics profiling revealed urogenital metabolic dysregulation in ccRCC, including increased lipid metabolism, altered mitochondrial respiration signatures, and elevated urinary lipid content. We identified three urinary protein biomarkers: serum amyloid A1 (SAA1), haptoglobin (HP), and lipocalin 15 (LCN15). Using a parallel reaction monitoring mass spectrometry workflow, we developed a rapid and sensitive assay and combined these markers into a diagnostic UrineScore. The UrineScore achieved 0.96 in an area under the receiver operating characteristic curve analysis in the discovery cohort, and 0.95 in an independent validation cohort. Together, these results support the feasibility of multi-omics-guided urinary biomarker discovery and represent a step toward accessible diagnostic platforms for ccRCC. - Source: PubMed
Publication date: 2026/08/11
Jonsson GustavOliveira TiagoHofmann MauraLemberger UrsulaStejskal KarelKrššáková GabrielaSakic IrmaNovatchkova MariaMereiter StefanGrabmann GerlindeKöcher ThomasKoglgruber RubinaKikic ZeljkoCamano Páez SoniaLuna Sanchez BárbaraDíez Nicolás VíctorRechberger Gerald NZüllig ThomasHagelkruys AstridEnglinger BernhardSchmidinger ManuelaPenninger Josef M - Histopathological growth patterns (HGPs) have emerged as prognostic and predictive biomarkers in colorectal liver metastases (CLM). The desmoplastic/encapsulating HGP (EHGP) is associated with improved survival after surgery, whereas the replacement HGP (RHGP) is associated with poorer outcomes. However, HGPs can only be reliably assessed postoperatively, limiting their use as preoperative biomarkers. A deeper molecular understanding of HGPs could inform biomarker development and therapeutic strategies, including approaches to promote EHGP. - Source: PubMed
Publication date: 2026/07/28
Escriva Conde MariaAndersson AxelVermeulen PeterNilsson MatsNyström Hanna - Periodontitis is a chronic inflammatory disease characterized by irreversible destruction of alveolar bone, periodontal ligament attachment, and supporting tooth structures. Emerging evidence suggests that periodontal tissue breakdown and regenerative failure are primarily driven by dysregulation of the local immune microenvironment rather than by direct bacterial insult. Therefore, conventional therapies focused primarily on microbial control are insufficient to restore immune homeostasis and functional regeneration of the cementum-periodontal ligament-alveolar bone complex. Effective periodontal regeneration requires coordinated infection management, immune modulation, oxidative stress clearance, and inflammatory microenvironment reprogramming to relieve the suppression of regenerative cells, particularly periodontal ligament stem cells. This review summarizes key regulatory networks of the periodontal immune microenvironment, with emphasis on macrophage polarization, neutrophil heterogeneity, and the imbalance between Th17 cells and regulatory T cells. We further discuss recent immune-engineering strategies for restoring periodontal homeostasis, including surface-modified biomaterials, ion-delivery systems, stem cell-derived extracellular vesicles, gene-editing technologies, and smart responsive therapeutic scaffolds. Advances in single-cell and spatial transcriptomics have revealed previously unrecognized functional subpopulations, such as NLRP3 macrophages and SAA1 fibroblasts, offering new opportunities for precision immunomodulation. Collectively, this review provides an integrated and translational framework for leveraging immune microenvironment-based interventions to achieve functional and predictable periodontal regeneration. - Source: PubMed
Zhang RuyiZhang HuachangZeng WenhuaZhao JiqingXia HaoZhang NanLi Keyi