SFRP2
- Known as:
- SFRP2
- Catalog number:
- Y213676
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- SFRP2
Related genes to: SFRP2
- Gene:
- SFRP2 NIH gene
- Name:
- secreted frizzled related protein 2
- Previous symbol:
- -
- Synonyms:
- SARP1, SDF-5, FRP-2
- Chromosome:
- 4q31.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-07-15
- Date modifiied:
- 2016-05-04
Related products to: SFRP2
Anti-SFRP2 AntibodyAntibodies: SFRP2 HOST: Goat Clonality: pAbBovine Secreted frizzled-related protein 2(SFRP2) ELISA kitCanine Secreted frizzled-related protein 2(SFRP2) ELISA kitCanine Secreted frizzled-related protein 2(SFRP2) ELISA kitCanis familiaris,Canis lupus familiaris,Dog,Secreted frizzled-related protein 2,SFRP2,sFRP-2Chicken secreted frizzled-related protein 2 (SFRP2) ELISA kit, Species Chicken, Sample Type serum, plasmaChicken Secreted frizzled-related protein 2(SFRP2) ELISA kitChicken Secreted frizzled-related protein 2(SFRP2) ELISA kitChicken Secreted frizzled-related protein 2(SFRP2) ELISA kit SpeciesChickenChicken SFRP2 (Secreted Frizzled Related Protein 2) ELISA KitChicken SFRP2 (Secreted Frizzled Related Protein 2) ELISA KitChicken,Gallus gallus,Secreted frizzled-related protein 2,SFRP2,sFRP-2Dog secreted frizzled-related protein 2 (SFRP2) ELISA kit, Species Dog, Sample Type serum, plasmaDog Secreted frizzled-related protein 2(SFRP2) ELISA kit Related articles to: SFRP2
- Cardiac fibrosis is increasingly recognized as a dynamic program that resolves into a terminal fibroblast fate, the matrifibrocyte, rather than a persistent myofibroblast state. Lineage-tracing and single-cell studies reveal that matrifibrocytes arise from activated myofibroblasts during late scar maturation, lose α-SMA and proliferative capacity, and adopt a cartilage-like ECM program (e.g., Comp, Chad, Thbs4, Sfrp2). Functionally, they stabilize collagen architecture, sustain tensile strength and shape an immune-quiescent, angiogenesis-restrained microenvironment. We synthesize evidence suggesting that TGF-β restraint (e.g., Smad7), matrix mechanics (YAP/TAZ), Wnt attenuation (Sfrp2), Comp-Notch3 feedback, and Thbs4-Atf6α ER-stress adaptation converge to establish or maintain this terminal state. We further summarize disease contexts beyond infarction, including pressure overload and valvular disease, where matrifibrocyte-like programs emerge and may contribute to chronic stiffening. Finally, we outline translational strategies that either accelerate matrifibrocyte maturation to secure scars after acute injury or reset terminal states via pharmacology or direct reprogramming to regress fibrosis. Framing matrifibrocytes as an adjustable endpoint reconciles structural integrity with functional recovery and highlights actionable checkpoints for precision anti-fibrotic therapy. - Source: PubMed
Zhang ZhentaoZhu Hua - Colorectal cancer screening programs are well-established worldwide, but most applied methods are invasive, have insufficient accuracy, or have a low uptake rate. Several studies have reported DNA methylation biomarkers as promising alternatives to the established diagnostic tools. However, the current reviews on the topic lack information on the exact location of the CpG sites in the analyzed biomarker. As adjacent CpG sites may exert distinct clinical effects, precise identification of the specific CpG sites analyzed is essential for establishing clinical relevance and achieving consensus across studies. This scoping review aimed to uncover the accessibility of CpG site information in the scientific literature, map the CpG sites of the markers, and summarize the accuracy data from studies reporting on the same group of CpG sites. We systematically searched MEDLINE®, EMBASE, and Scopus, and the last search was conducted on the 13th of March 2025. A total of 6180 identified records were screened in Covidence, resulting in the inclusion of 149 articles. Four (2.7%) papers held precise CpG information. Locations of the CpG sites were obtained for additionally 109 (73.2%) papers by running a BLAST search using oligonucleotide sequences from the papers. For the remaining 36 (24.1%) papers without any information to locate the CpG sites, 26 used commercial kits. The three most frequently studied genes were SEPTIN9, SDC2, and SFRP2. We mapped the CpG sites of these to identify recurring sites across the studies. Sixteen of 22 papers analyzing SEPTIN9 had three CpG sites in common, seven of 19 papers analyzing SDC2 had consensus on a single CpG site, while seven of 13 studies reporting on SFRP2 had analyzed eight identical CpG sites. Lastly, we grouped all studies based on whether they targeted the same group of CpG sites within each gene. For genes examined in at least two papers, we summarized the reported accuracy measurements by presenting the average, minimum, and maximum values for each CpG group. This scoping review identifies a profound lack in the reporting of the CpG sites analyzed for non-invasive detection of CRC, which poses a challenge for the comparison of findings across studies. - Source: PubMed
Publication date: 2026/05/05
Bendixen Kamilla KoldingPoulsen Winnie RoerbaekGundel-Reimer Luna KatrinePetersen Rasmus KoefoedSoerensen Mette - Diabetic kidney disease (DKD) is characterized by renal lipid accumulation, but the molecular mechanisms underlying this lipotoxic phenotype remain unclear. Secreted frizzled-related protein 2 (SFRP2) has been implicated in metabolic regulation, yet its role in renal cholesterol homeostasis and DKD pathogenesis is unknown. - Source: PubMed
Publication date: 2026/04/15
Lv DanLin ZiyueYang JiakunLi WuchaoWu KeqianPeng RuiLiu HandengZha HeRuan Xiong ZhongLiao XiaohuiSun YanZhang Zheng - Mammalian palates are composed of the anterior hard palate and the posterior soft palate. However, the correlation of the genesis, pattern formation, and morphogenesis between the hard and soft palates remains elusive. - Source: PubMed
Publication date: 2026/03/20
Wang BiyingXue JunyuanBian YufanDeng JiaminLiu BoLi NanZhu LeiXiao JingLiu ChaoLiu Han - Cardiac fibroblast (CF) differentiation into myofibroblasts is a crucial driver of cardiac fibrosis, leading to myocardial stiffness and eventually impairing heart function. Cardiomyocyte-fibroblast intercellular communication has emerged as a key regulatory way for CF activation and the fibrotic response. However, the molecular mechanisms linking cardiomyocyte secretomes to CF activation within heart failure remain poorly understood. Here, we identified a stress-responsive protein Maf1 in cardiomyocytes as a central regulator of CF activation in both in vivo and in vitro models of cardiac fibrosis. Maf1 overexpression (cardiomyocyte-specific Maf1 overexpression mice, Maf1 cOE) attenuated CF proliferation, ECM protein expression, and myofibroblast differentiation, while Maf1 loss-of-function (Maf1 knockout mice, Maf1-KO) exacerbated cardiac fibrosis. Notably, Maf1 directly suppresses the expression and secretion of Sfrp2 by affecting its promoter DNA methylation through DNA methyltransferase 1 (Dnmt1), which is essential for promoting CF activation and fibrosis. Sfrp2 overexpression or Sfrp2 recombinant protein treatment exacerbates TGFβ1-induced fibrosis, while silencing Dnmt1 reverses the upregulation of Sfrp2 by Maf1. These findings identify Maf1 as a pivotal link between cardiomyocyte secretomes and fibrosis, suggesting it as a potential therapeutic target to mitigate fibrosis and enhance cardiac recovery during heart failure. - Source: PubMed
Li JiayongXue RuicongLiang WeihaoZhen ZheChen ChenWang YilongWu YuzhongLi JiaXie ZengshuoHuang YuwenYang YunyaoDai GangFan WendongFang RongZhang LiliYu YuanHuang Zhan-PengDong YugangLin Kai-YangHuang PeisenLiu Chen