Ask about this productRelated genes to: FZD5 Blocking Peptide
- Gene:
- FZD5 NIH gene
- Name:
- frizzled class receptor 5
- Previous symbol:
- C2orf31
- Synonyms:
- HFZ5, DKFZP434E2135
- Chromosome:
- 2q33.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-09-17
- Date modifiied:
- 2015-09-11
Related products to: FZD5 Blocking Peptide
Related articles to: FZD5 Blocking Peptide
- Idiopathic pulmonary fibrosis (IPF) is a fatal interstitial lung disease driven by persistent activation of pulmonary myofibroblasts, but the regulatory mechanisms sustaining this pathological state remain incompletely understood. Using single-cell RNA sequencing (scRNA-seq), we identified SFRP2 (secreted frizzled related protein 2) as a critical mediator of profibrotic myofibroblasts in IPF lungs. Functional studies revealed that SFRP2 acted in an autocrine manner to promote myofibroblast activation and extracellular matrix (ECM) production. Mechanistically, SFRP2 activated FZD5-mediated non-canonical WNT-Ca signaling, leading to PPP3/calcineurin-dependent translocation of PINK1 from the outer to the inner mitochondrial membrane (IMM), where it was degraded, thereby inhibiting PINK1-mediated mitophagy. Furthermore, therapeutic intervention with AAV6-sh, SFRP2-neutralizing antibody, or the autophagy inducer rapamycin significantly ameliorated lung fibrosis in bleomycin (BLM)-induced mouse models. Our results define a novel autocrine SFRP2-mitophagy regulatory axis that perpetuates myofibroblast activation and represents a promising therapeutic target for pulmonary fibrosis.: AAV: adeno-associated virus; BLM: bleomycin; CQ: chloroquine; ECM: extracellular matrix; FZD5: frizzled class receptor 5; H&E: hematoxylin and eosin; IHC: immunohistochemical; IMM: inner mitochondrial membrane; IPF: idiopathic pulmonary fibrosis; Micro-CT: micro-computed tomography; mtROS: mitochondrial reactive oxygen species; PMLFs: primary mouse lung fibroblasts; qPCR: quantitative real-time PCR; scRNA-seq: single-cell RNA sequencing; SFRP2: secreted frizzled related protein 2; TEM: transmission electron microscopy; ∆Ψm: mitochondrial membrane potential. - Source: PubMed
Publication date: 2026/03/15
Lin YingyingLei TianxiangJia YifanYao MeilingWang XiaofengHuang ShaojieWang ZhongxingLai Xiaofan - Increasing evidence suggests that epigenetic regulation plays a central role in chronic rhinosinusitis pathogenesis, heterogeneity, and treatment response. This review summarizes current knowledge of epigenetics in CRS pathogenesis, their role in endotype differentiation, and potential as diagnostic and therapeutic targets. - Source: PubMed
Publication date: 2025/11/27
Kumar NitishBrar TriptiLal Devyani - Diabetes mellitus is a major independent determinant of cardiovascular morbidity. Therefore, we evaluated whether a molecular RNA panel comprising and could facilitate the early detection and discrimination of ischemic heart disease in individuals with type 2 diabetes mellitus. - Source: PubMed
Publication date: 2025/10/31
Sedkey Eslam SMatboli MarwaSeadawy Mohamed GHegazy Marwa G A - Cesarean section (CS) scar tissue fibrosis and decreased muscle density increase the risk of uterine rupture and placental implantation in subsequent pregnancies. Given the potent anti-fibrotic and regenerative properties of human amniotic mesenchymal stem cells (hAMSCs), this study investigated their therapeutic potential in repairing uterine scars in a rat model. A full-thickness uterine wall excision model was established to mimic CS scarring. hAMSCs were transplanted at the edge of the incision. Myometrial thickness and collagen deposition within the scar were assessed histologically using hematoxylin and eosin (H&E) and Masson's staining. Immunohistochemistry evaluated the expression of MMP8, TGF-β1, VEGFA, and α-SMA within the scar region. mRNA transcriptome sequencing and quantitative real-time polymerase chain reaction (qRT-PCR) were employed to explore possible mechanisms. A total of 110 rats were used in the study, 30 in the sham group, 40 in the phosphate-buffered saline (PBS) control group and 40 in the hAMSCs treatment group. Compared with the PBS group, the hAMSCs group exhibited a 35% reduction in collagen fiber area and a 28% increase in smooth muscle cell density ( < 0.05). The MMP8, VEGFA, and α-SAM expressions in the uterine scar area of rats increased, whereas the TGF-β1 expression decreased ( < 0.05). Transcriptome sequencing and real-time fluorescence quantitative PCR results showed that the expression levels of Wnt4, Fzd5, Wnt5a, and PPARD genes were lower in the uterine scar region of rats in the hAMSCs group compared with those in the PBS group. Transplantation of hAMSCs inhibits scar formation in uterine wounds and promotes regeneration of smooth muscle tissue and neovascularization, which in turn promotes uterine wound repair. This effect may be related to the activation of Wnt pathway and the inhibition of PPARD gene expression. - Source: PubMed
Publication date: 2025/10/31
Li CaixiZhao FengSong JiaZhang TingYang RuiXiao YiZheng YujiaSun JingliChen Zhenyu - Frizzled (FZD) proteins are the principal receptors of the Wnt signaling pathway. However, whether Wnt ligands induce FZD endocytosis and degradation remains elusive. The transmembrane E3 ubiquitin ligases ZNRF3 and RNF43 promote the endocytosis and degradation of FZD receptors to inhibit Wnt signaling, and their function is antagonized by R-spondin (RSPO) proteins. However, the dependency of RSPO-ZNRF3/RNF43-mediated FZD endocytosis and degradation on Wnt stimulation, as well as the specificity of this degradation for different FZD, remains unclear. Here, we demonstrated that Wnt specifically induces FZD5/8 endocytosis and degradation in a ZNRF3/RNF43-dependent manner. ZNRF3/RNF43 selectively targets FZD5/8 for degradation upon Wnt stimulation. RSPO1 enhances Wnt signaling by specifically stabilizing FZD5/8. Wnt promotes the interaction between FZD5 and RNF43. We further demonstrated that DVL proteins promote ligand-independent endocytosis of FZD but are dispensable for Wnt-induced FZD5/8 endocytosis and degradation. Our results reveal a novel negative regulatory mechanism of Wnt signaling at the receptor level and illuminate the mechanism by which RSPO-ZNRF3/RNF43 regulates Wnt signaling in human cells, which may provide new insights into regenerative medicine and cancer therapy. - Source: PubMed
Publication date: 2025/10/10
Luo DongZheng JingLv ShuningSheng RenChen MaorongHe XiZhang Xinjun