Ask about this productRelated genes to: Bmp10 antibody
- Gene:
- BMP10 NIH gene
- Name:
- bone morphogenetic protein 10
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 2p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-04-16
- Date modifiied:
- 2019-04-23
Related products to: Bmp10 antibody
Related articles to: Bmp10 antibody
- : Pacemakers enable continuous long-term surveillance of atrial fibrillation detected by implanted devices. Circulating biomarkers reflecting endothelial dysfunction, inflammation, and myocardial stress may help identify patients at risk for atrial fibrillation (AF) progression and higher arrhythmic burden. : This analysis included patients from the prospective ACaSA study (NCT05127720) with a dual chamber pacemaker (Microport BOREA DR or TEO DR) and monitored weekly via remote monitoring technology (SMARTVIEW). Individuals with permanent AF or single-chamber systems were excluded. Baseline plasma concentrations of angiopoietin-2 (ANGPT2), growth differentiation factor-15 (GDF-15), fibroblast growth factor-23 (FGF-23), bone morphogenetic protein-10 (BMP10), and tumor necrosis factor-related apoptosis-inducing ligand receptor-2 (TRAIL-R2) were quantified using enzyme-linked immunosorbent assays. N-terminal pro-B-type natriuretic peptide (NT-proBNP) was measured using electrochemiluminescence immunoassay. Biomarkers were log-transformed, with values below assay detection limits imputed at half the lower limit of detection. Two endpoints were assessed following a 30-day blanking period: (1) progression to persistent AF, defined as ≥7 consecutive days with >99% daily AF burden, analyzed using Cox regression; and (2) AF burden, calculated as total AF time normalized to monitored days and categorized as <25%, 25-75%, or >75%, analyzed using multinomial logistic regression. Multivariable models were adjusted for age, sex, heart failure, diabetes, and prior myocardial infarction; Cox models were limited to age, sex, and heart failure due to fewer events. : A total of 223 patients were included (median age 75 years; 37.2% women). During follow-up, 28 patients (13.3%) progressed to persistent AF. Higher baseline ANGPT2 was the strongest predictor of progression (HR per doubling 1.83, 95% CI 1.27-2.66, = 0.001), followed by GDF-15 (HR 1.52, 95% CI 1.03-2.24, = 0.036). In the burden analysis, ANGPT2 demonstrated a pronounced graded relationship with arrhythmic load, with markedly increased odds of high (>75%) AF burden (OR 8.31, 95% CI 2.63-26.26, < 0.001). GDF-15 independently predicted both medium (OR 2.05, = 0.025) and high burden (OR 2.32, = 0.037). NT-proBNP displayed a borderline association with high burden (OR 2.02, = 0.061). No significant associations were observed for FGF-23, BMP10, or TRAIL-R2. : In continuously monitored pacemaker patients, ANGPT2 and GDF-15 emerged as key biomarkers associated with AF disease severity. ANGPT2 was strongly linked to both progression to persistent AF and high AF burden, whereas GDF-15 consistently predicted higher AF burden and also contributed to risk of progression. These findings highlight endothelial and inflammatory pathways as potential markers of atrial disease progression. - Source: PubMed
Publication date: 2026/04/16
Bilgeri ValentinSpitaler PhilippGavranovic-Novakovic JasminaDolejsi TheresaRockenschaub PatrickMessner MoritzZaruba Marc MichaelBarbieri FabianAdukauskaite AgneStühlinger MarkusPfeifer Bernhard ErichLacaita PietroFeuchtner GudrunWilleit PeterBauer AxelDichtl Wolfgang - Dilated cardiomyopathy (DCM) is a primary myocardial disorder characterized by progressive ventricular dilatation and impaired myocardial systolic contractility, and it represents the most common form of cardiomyopathy globally. DCM drives a substantial worldwide disease burden, thus presenting a formidable and persistent challenge to global public health systems. The pathogenesis of DCM is marked by extreme etiological heterogeneity: 30%-50% of cases have a familial origin, with genetic determinants serving as the core driver of disease onset and progression. With the rapid advancement and widespread application of next-generation sequencing (NGS) technologies, a growing repertoire of DCM-causative genes has been successfully identified. These genes encode key functional proteins that regulate multiple core physiological processes in cardiomyocytes, including sarcomeric structure maintenance, intracellular signal transduction, and myocardial energy homeostasis. DCM-causing genes can be classified into multiple categories according to their functions. Sarcomeric protein genes (such as TTN, MYH7, and TNNT2) disrupt sarcomere assembly and contractile function through mechanisms such as haploinsufficiency and the toxic peptide hypothesis; mutations in nuclear membrane protein genes (such as LMNA and EMD) cause abnormal nuclear structure and disordered mechanotransduction signals; ion channel genes (such as SCN5A, CACNA1C, and RYR2) affect electrophysiological balance and calcium handling; desmosome-related genes (such as DSC2 and DSP) are associated with abnormal cell junctions and dysregulation of the Wnt/β-catenin pathway; KLF13, ETS1, and BMP10 are possible candidate genes for DCM with limited research; loss of function of RBM20 leads to abnormal splicing of TTN, CamkIIδ, RyR2, etc. and causes nuclear import defects as well as cytoplasmic RBM20-RNP granule toxicity, thereby driving ventricular dilation. These genes drive myocardial remodeling through common signaling pathways (such as ERK and TGF-β). Potential treatment strategies include gene-level interventions, targeted pathway inhibitors, and myosin activators. However, genetic heterogeneity results in a narrow applicable population for single-gene therapies. Future research needs to shift from targeting individual genes to improving the common pathological environment to achieve broad-spectrum treatment. Exploring upstream prevention of mutations or activation of endogenous repair mechanisms provides new directions for the treatment of DCM. - Source: PubMed
Publication date: 2026/03/28
Zhang XiaoZhang XinyuChen YunruHuan NaWang ChenglongZhang Dawu - Hepatic stellate cells (HSCs) and their derived cancer-associated fibroblasts (CAFs) are integral to the development, progression, and prognosis of hepatocellular carcinoma (HCC). However, the mechanisms underlying the transformation of HSCs into CAFs and their subsequent roles in HCC remain incompletely understood. The expression of METTL3 was analyzed in fibroblasts infiltrating into human HCC specimens compared to adjacent non-tumor tissues. The effects of HSC-specific METTL3 deficiency on HCC were analyzed by orthotopically transplanting hepatoma cells into the mouse fibrotic liver and directly or indirectly co-culturing hepatoma cells with HSCs. We found that the expression of METTL3, the methyltransferase responsible for RNA N6-methyladenosine (m6A) modification, was downregulated in fibroblasts infiltrating into HCC compared to that of adjacent non-tumor tissues. Orthotopical transplantation of HCC cells in fibrotic liver showed that HSC-specific METTL3 deficiency significantly increased tumor burden. Meanwhile, conditioned medium treatment and mixed co-culture confirmed that METTL3 deletion in HSCs promoted HCC proliferation and migration in vitro, demonstrating that METTL3 deficiency in HSCs accelerated HCC progression in fibrotic liver. Mechanistically, METTL3 deficiency reduced m6A modification and expression of BMP10, a known tumor suppressor. Similar to the effects of METTL3 deficiency, BMP10 knockdown also promoted hepatoma cell growth, while recombinant BMP10 (rBMP10) inhibited it. Overexpression of BMP10 or addition of rBMP10 mitigated the tumor-promoting effects of METTL3-deficient HSCs. BMP10's effects were mediated through SMAD1/5/8 phosphorylation. Our study reveals a novel crosstalk between HSCs and hepatoma cells via the METTL3/m6A-BMP10-SMAD1/5/8 axis, suggesting a potential therapeutic target for HCC. - Source: PubMed
Publication date: 2026/04/24
Yu ShanshanZhang YiwangLi YanliPan LijieLiang XiaoqiMeng WanruDong ShuaiSun YuetongLiu XiaoYe LinsenZhang QiXu Yan - To integrate clinical and preclinical evidence on insulin-like growth factor-binding protein-7 (IGFBP7) in heart failure (HF) and identify key priorities for advancing IGFBP7-targeted therapies toward human translation. - Source: PubMed
Publication date: 2026/04/21
El-Qendouci MaissaChelu RalucaAbdellatif MahmoudJhund Pardeepde Boer Rudolf ASuthahar Navin - Relative fat mass (RFM), an adiposity index derived from waist circumference and height, has emerged as a strong and consistent marker of cardiometabolic risk. However, evidence on its association with incident stroke is limited. This study aimed to evaluate the associations of RFM with incident stroke and its subtypes. - Source: PubMed
Publication date: 2026/03/18
Suthahar NavinYang YiqianGansevoort Ron TDamman KevinRienstra MichielBergman Richard NBakker Stephan Jlde Boer Rudolf A