Ask about this productRelated genes to: BMP10 protein
- 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 protein
Related articles to: BMP10 protein
- - Source: PubMed
Publication date: 2026/08/05
Suthahar NavinLau Emily S - Hereditary hemorrhagic telangiectasia (HHT) is a rare autosomal dominant vascular disorder characterized by mucocutaneous telangiectases and visceral vascular malformations, leading to recurrent bleeding, iron-deficiency anemia, and organ complications. Pulmonary, cerebral, and hepatic involvement are major determinants of morbidity and mortality. Management has traditionally relied on local and interventional approaches, which are largely palliative and do not address underlying disease mechanisms. New insights in HHT pathophysiology, particularly in the dysregulated BMP9-BMP10/ENG/ALK1 pathway, which is fundamental to the angiogenesis process, have enabled the development of targeted systemic therapies. Although no systemic drug is specifically approved for HHT, antifibrinolytics, anti-angiogenic agents, mTOR and AKT inhibitors, and immunomodulatory drugs have shown variable efficacy in selected patients. This review summarizes current evidence on systemic therapies and ongoing clinical trials, highlighting their potential to complement existing strategies and move toward disease-modifying approaches. - Source: PubMed
Publication date: 2026/08/21
Castañeda-Pérez SabelaOrdieres-Ortega LucíaAlves-Pereira Eide DianaRiera-Mestre Antoni - Here, we report the identification of a previously unrecognized population of tumor-induced podoplanin-positive (PDPN) cells in clear-cell renal cell carcinoma (ccRCC) that exhibit features of under-differentiated lymphatic endothelial cells (LECs). These PDPN cells lack a complete repertoire of canonical LEC markers, including VE-cadherin, LYVE1, and VEGFR3, and fail to form functional lymphatic vessels, indicating a dysplastic phenotype. We termed these cells dysLECs and found that these cells are induced by BMP10 produced specifically by tumor cells. In turn, dysLECs secrete CXCL13, which promotes tumor cell proliferation and metastasis. Ligand-receptor analyses revealed a highly tumor-specific reciprocal signaling circuit: kidney tubule cells deficient in the von Hippel-Lindau () tumor suppressor gene uniquely express BMP10, a TGF-β family cytokine, whereas its receptor ALK1 is restricted to dysLECs; conversely, dysLECs produce CXCL13, while mutant kidney tubule cells uniquely express its receptor, CXCR5. Pharmacological inhibition of ALK1 reduced CXCL13 production and suppressed the hyperplastic phenotype of mutant tumor cells in vivo, whereas BMP10 neutralization inhibited tumor growth and metastasis in an orthotopic ccRCC xenograft model. Collectively, these findings identify a dysplastic population of PDPN lymphatic-like endothelial cells and define a tumor-specific BMP10-CXCL13 signaling axis that drives ccRCC progression, uncovering a previously unrecognized therapeutic vulnerability in this disease. - Source: PubMed
Publication date: 2026/08/04
Nguyen Tuong-ViNguyen-Tran Hieu-HuyNguyen Thi-NgocHsu Tien - Cognitive impairments, particularly in the domain of memory, are core and enduring features of schizophrenia. Bone morphogenetic proteins (BMPs), members of the transforming growth factor-β superfamily, are involved in neurodevelopment and synaptic plasticity, but few studies have investigated their relevance to cognitive deficits in schizophrenia. - Source: PubMed
Publication date: 2026/07/17
Yang QunHou JieJiang FeiDing YaqinJin SichangYang XiaoyuLi ShuangWang PeijuanTian QingZhang Xiaobin - Combined formulations represent 38% of pesticide products due to economic incentives. The herbicide combination of fluroxypyr-meptyl (FPMH) and carfentrazone-ethyl (CE) is widely used in agriculture with concurrent residue detection in aquatic environments indicating ecological risks. However, their toxic effects on aquatic organisms remain poorly understood. This study investigated the developmental toxicity of individual and combined FPMH and CE exposures in zebrafish embryos through acute toxicity tests following the OECD standard. We applied morphological, biochemical, gene-expression and molecular docking analyses to assess cardiotoxicity. The results showed that the 96 h-LC values were 3.660 mg/L for FPMH, 0.218 mg/L for CE and 0.766 mg/L for their mixture at a 1:1 equitoxic ratio. Moreover, the additive index analysis yielded an AI value of -0.5320 (<0), indicating an antagonistic interaction during co-exposure. All exposures significantly impaired embryonic development, increasing malformation rates and reducing body length. Additionally, cardiac abnormalities included pericardial edema, enlarged pericardial area, increased sinus venosus-bulbus arteriosus (SV-BA) distance, cardiac linearization and decreased heart rate. Mechanistically, we found that zebrafish embryos exposed to FPMH and CE both individually and in combination exhibited apoptosis and oxidative stress. RT-qPCR and GGE biplot analysis revealed stable aberrant expression of cardiac (Bmp10) and apoptotic (TNF-α, Fas, FADD) genes, while molecular docking revealed high binding affinity of these proteins for FPMH and CE both individually and in combination. In summary, this study examined the developmental toxicity and apoptosis- and oxidative stress-mediated cardiotoxicity in zebrafish embryos following exposure to FPMH and CE either individually or in combination, providing new insights for environmental risk assessment of FPMH, CE and their combined formulations. - Source: PubMed
Publication date: 2026/07/14
Dong LiSu XiaoTingYang XuJiangLiu ShiYingSuo LiangHaoZhang JieXie JiaFarooq SaqibFan YongMei