Ask about this productRelated genes to: PDGFRB antibody
- Gene:
- PDGFRB NIH gene
- Name:
- platelet derived growth factor receptor beta
- Previous symbol:
- PDGFR
- Synonyms:
- JTK12, CD140b, PDGFR1
- Chromosome:
- 5q32
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-10-05
Related products to: PDGFRB antibody
Related articles to: PDGFRB antibody
- Phenotypic switching of vascular smooth muscle cells (VSMCs), leading to neointima formation, is a main cause of in-stent restenosis after coronary stent implantation, resulting in poor patient prognosis. Inhibition of VSMC proliferation, migration, and synthetic phenotype transition holds promise for preventing and treating neointimal hyperplasia and restenosis. GW0742, a peroxisome proliferator-activated receptor (PPAR)-β/δ agonist, has been reported to suppress atherosclerosis and myocardial ischemia-reperfusion injury. However, its role in neointima formation has not been previously studied. In this study, we found that GW0742 significantly inhibited carotid artery injury-induced neointimal hyperplasia in mice. In vitro experiments including cell counting, EdU staining, and proliferation marker detection revealed that GW0742 markedly suppressed Platelet-derived growth factor-BB (PDGF-BB)-induced proliferation of human aortic smooth muscle cells (HASMCs). Flow cytometry analysis showed that GW0742 treatment arrested cells in the G2/M phase. Transwell assays demonstrated that GW0742 inhibited HASMCs migration. Moreover, GW0742 reduced the expression of migration-associated proteins matrix metalloproteinases 2 (MMP2) and matrix metalloproteinases 9 (MMP9), while increasing contractile markers alpha-smooth muscle actin (α-SMA) and calponin 1 (CNN1), suggesting that GW0742 suppresses HASMC proliferation, migration, and phenotypic switching, thereby preserving the contractile phenotype. RNA sequencing revealed that GW0742 regulates fatty acid metabolism by upregulating fatty acid binding protein 3 (FABP3) expression to counteract PDGF-BB-induced VSMC phenotypic switching. Knockdown of FABP3 significantly abrogated the inhibitory effects of GW0742 on VSMC proliferation, migration, and synthetic phenotype transition. Taken together, our findings demonstrate that GW0742 upregulates FABP3 expression, leading to the inhibition of VSMC proliferation, migration, and phenotypic switching, and ultimately suppressing neointima formation. These results underscore the therapeutic potential of GW0742 for the prevention and treatment of vascular restenosis. - Source: PubMed
Publication date: 2026/08/12
Wang XueshengChen JingjieHuo BoWu XingliangLin WenxinJiang Ding-ShengZhang Yu-SongFeng XinGong Fu-Han - [This corrects the article DOI: 10.1016/j.heliyon.2025.e43767.]. - Source: PubMed
Publication date: 2025/12/05
Yi HaoLiu Hao-HanDing Jia-TongZhou Hao-NanHuang Hao-YuLiu JiangHuang Ying-FengZhou Tai-ChengZong Zhen - Platelet-derived growth factors (PDGFs) and their cognate receptors (PDGFRα/β) play critical roles in breast cancer progression and metastasis. This review summarizes current evidence of PDGF ligand and receptor expression patterns, oncogenic functions, prognostic significance and therapeutic targetability, with a specific focus on small molecule inhibition. PDGF-PDGFR signaling is known to contribute to epithelial to mesenchymal transition, cancer stem cell maintenance, desmoplasia, angiogenesis, and immune modulation. Additionally, the four PDGF ligands have distinct oncogenic functions. PDGFA and PDGFB have been implicated in breast cancer associated brain metastasis, while PDGFC has been shown to play a crucial role in fibroblast activation. PDGFD, while less studied, may activate epithelial to mesenchymal transition in breast cancer. High expression of PDGFA, PDGFB, PDGFC, and stromal PDGFRβ correlate with poor patient survival, highlighting their potential as candidate biomarkers. We specifically focus on evaluating current therapeutic strategies which target the PDGF-PDGFR axis, including neutralizing antibodies, aptamers, and small molecule inhibitors, which show preclinical promise but limited clinical success in breast cancer to date. We discuss future research directions with emphasis on identifying selective inhibitors, utilizing PDGF-PDGFR signaling components for patient stratification, and combination with immunotherapies. - Source: PubMed
Publication date: 2026/08/07
Reardon Jesse JMossing Alexis APackard Rebecca LShah SajitaSizemore Gina M - Liver fibrosis is a progressive pathological process driven by liver injury, including viral hepatitis and metabolic dysfunction-associated steatohepatitis (MASH), and can progress to cirrhosis, liver failure, and hepatocellular carcinoma (HCC). Hepatocyte-hepatic stellate cell (HSC) crosstalk plays a central role in disease progression, but its regulatory mechanisms remain incompletely understood. - Source: PubMed
Publication date: 2026/08/07
Zhou Ji-ChaoXu An-JianMiao JingXu Rui-BingZhang Zhi-MengFan Ying-LiYu Jin-MeiYu Jiao-JiaoYuan Hong-YuLi Ping-PingCui BingZhang Xiao-Wei - Infantile myofibroma (IM) is the most common congenital fibrous tumor of infancy, originating from fibroblasts and myofibroblasts and present at birth in approximately 50%-60% of cases. Solitary IMs most often develop in the head and neck, less frequently on the trunk or extremities, and usually have an excellent prognosis in the absence of visceral involvement. Clinically, IM appears as a painless, firm, bluish-purple, freely mobile nodule and may occasionally show ulceration or skin atrophy, clinically mimicking hemangioma. Imaging typically shows well-defined masses with low-flow or peripheral vascularity, distinguishing them from highly vascular hemangiomas. Although solitary lesions may spontaneously regress within 18-24 months, surgical excision is advised when diagnosis is uncertain, functional risk exists, or for cosmetic or psychosocial reasons. Multicentric IM without visceral involvement also has a favorable outcome, whereas lesions with visceral involvement carry significantly higher morbidity and mortality. Mutations in and, less commonly, are reported in IM and may guide future targeted therapies. In the absence of standardized guidelines, management must be individualized, with options including observation, surgical excision, and chemotherapy for extensive or visceral disease. Regular clinical and imaging follow-up is essential until lesion stabilization or regression is confirmed. Here, we present a female neonate with a scalp IM. Persistent ulceration, recurrent bleeding, inability to definitively exclude malignancy on imaging, and significant maternal distress warranted the decision for surgical excision. This case emphasizes the importance of individualized care in IM, guided by current literature on presentation, pathology, and treatment. - Source: PubMed
Publication date: 2026/08/05
Jarrar Salma IAltuntas AysePopov Sergey DAlRayahi Jehan ABabiker Haithem E