Ask about this productRelated genes to: MFAP4 antibody
- Gene:
- MFAP4 NIH gene
- Name:
- microfibril associated protein 4
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 17p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-11-17
- Date modifiied:
- 2017-05-16
Related products to: MFAP4 antibody
Related articles to: MFAP4 antibody
- Colorectal cancer (CRC) is a leading cause of cancer mortality. The extracellular matrix (ECM) plays a critical role in tumor progression, and its associated genes may serve as prognostic biomarkers. This study investigated three ECM-related genes, CILP, MFAP4, and MMRN1, to evaluate their expression and clinical significance in CRC development. - Source: PubMed
Publication date: 2026/04/25
Golestannejad ErfanKalantary-Charvadeh AshkanKarimi JamshidKhodadadi Iraj - Response rates to single-agent PD-1/PD-L1 blockade in bladder cancer remain modest, underscoring the need for alternative, targetable axes. Microfibril-associated protein-4 (MFAP4) is dysregulated in cancers, yet its role in bladder cancer is unclear. - Source: PubMed
Publication date: 2026/05/06
Zhou YingchenHuang YingQiJian NiZhu YizhunZhang CongyuYangyang Liang YuhongLi DandanZhang YatongLiu FangxianHuang WeirenChen Wei - Endothelial plasticity, the capacity of endothelial cells (ECs) to reversibly alter their phenotype in response to environmental cues, typically enables adaptive vascular remodeling and tissue homeostasis. In diabetes, this plasticity becomes maladaptive, driving pathological transitions across interconnected axes: dysregulated angiogenesis with barrier destabilization, inflammatory reprogramming through immune-endothelial crosstalk, metabolic dysfunction spanning mitochondrial stress to senescence, and endothelial-to-mesenchymal transition with fibrosis. In this review, we synthesize mechanistic insights across endothelial state transitions and highlight how single-cell approaches have reframed diabetic vascular disease as a disorder of maladaptive endothelial plasticity. By integrating single-cell insights from diabetic mouse models and human patient samples, we demonstrate that restoring adaptive endothelial plasticity requires coordinated multi-dimensional intervention targeting the intersecting pathways that perpetuate pathological transitions, timed to disease stage and calibrated to vascular bed-specific context. For example, combining metabolic therapies such as GLP-1 receptor agonists or SGLT2 inhibitors with anti-inflammatory agents targeting IL-17A or IL-1β, pairing anti-VEGF treatments with inhibitors of MFAP4 or ANGPTL4 to overcome angiogenic bypass pathways, or coupling senolytics, such as UBX1325, with anti-fibrotic strategies like TGF-β or SETD7 inhibition to prevent irreversible EndoMT. We identify candidate therapeutic targets across angiogenic, inflammatory, metabolic, and fibrotic domains, and highlight critical knowledge gaps, most notably the limited characterization of human diabetic ECs, that must be addressed to translate these insights into effective clinical strategies for preventing diabetic vascular complications. - Source: PubMed
Publication date: 2026/05/06
Alnuaimi Noura SLößlein LenaMousa MiraKhader Thanumol AbdulAlkhaaldi AyeshaAzzam Sarah KVan Craenenbroeck Amaryllis HAshraf Syed SalmanCarmeliet PeterAlsafar Habiba - This study aimed to investigate the role of the FBXW7/SPI1/MFAP4 axis in pulmonary arterial hypertension (PAH). - Source: PubMed
Publication date: 2026/03/31
Jiang ZhenzhuXiao BinlanHu ZheLi YuanmaoZhang HangPeng Haiyan - - Source: PubMed
Publication date: 2026/04/20
Zhang WenxinDai LiangliangLuo MingzhiShi Honglei