Ask about this productRelated genes to: Ctsd Blocking Peptide
- Gene:
- CTSD NIH gene
- Name:
- cathepsin D
- Previous symbol:
- CPSD
- Synonyms:
- CLN10
- Chromosome:
- 11p15.5
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2014-11-18
Related products to: Ctsd Blocking Peptide
Related articles to: Ctsd Blocking Peptide
- Cadmium (Cd) is a persistent environmental pollutant that poses a significant health risk to humans and animals, with acute exposure known to induce kidney injury. Fucoidan (Fc), a natural bioactive polysaccharide derived from brown algae, exhibits diverse biological activities; however, its potential to protect against Cd-induced kidney damage and the underlying mechanisms remain unclear. In this study, we investigated the effects of Fc on Cd-induced renal injury in vitro and further explored the role of transcription factor EB (TFEB) in regulating autophagy in its protective mechanism. Our results demonstrate that in Cd-exposed porcine kidney cells (PK-15), Fc suppressed the expression of renal inflammatory factors (TNF-α, IL-1β) and kidney injury markers (NGAL, NTN-1, KIM-1), reduced reactive oxygen species (ROS) production, and downregulated apoptosis-related proteins (cleaved caspase-3 and cleaved caspase-9). Mechanistically, Fc upregulated TFEB protein expression, enhanced the levels of lysosomal function-related proteins (Cathepsin B, CTSB; Cathepsin D, CTSD), and reversed Cd-induced autophagic flux blockade. Importantly, TFEB silencing abolished the protective effects of Fc. Collectively, these findings suggest that Fc exerts renoprotective effects against Cd-induced injury by restoring autophagic flux, a process that involves TFEB. - Source: PubMed
Publication date: 2026/05/13
Qu HaoboZhao XiaoyuWang YifanMao SichaoChen XingxiangHuang KeheXu Xinyi - Clearance of cerebral Aβ was primarily mediated by the brain endothelial transporters including LRP1. The regulatory mechanism of LRP1 expression remained unclear. - Source: PubMed
Li Zhi-JunYang ZhaoZhao DanQiu Yi-HuaWan Wen-YuHuang Zeng-KangTian LiQi Rui-QunLiu Hong-GuangChen Yu-HuaMin Dong-YuXu Xiao-QianZhao Wei-Dong - Per- and polyfluoroalkyl substances (PFAS) are persistent pollutants linked to breast cancer (BC), but their role in perineural invasion (PNI) of triple-negative breast cancer (TNBC) is unclear. Cathepsin D (CTSD), a lysosomal protease, is hypothesized to mediate PFAS-induced PNI, though systematic evidence is lacking. We integrated multi-omics data from TCGA-BRCA, METABRIC, and single-cell RNA-seq datasets. Analyses included differential gene expression, Mendelian randomization, consensus clustering, and machine learning for prognostic modeling. Single-cell analyses were performed using Seurat, Monocle2, and CellChat. GraphBan screened natural CTSD-binding compounds, with binding affinity evaluated by molecular docking and dynamics simulations. Experimental validation included immunohistochemistry, immunofluorescence, Transwell, and Western blot assays. We identified 5 PFAS-associated PNI-related genes (PPGs), with CTSD central to TNBC PNI. PPG-based molecular subtyping revealed a high-risk subgroup exhibiting enhanced epithelial-mesenchymal transition (EMT) activity, proliferation capacity, and significantly poorer overall survival. The PPG-based prognostic model effectively stratified patient outcomes and immunotherapy response. Mendelian randomization confirmed a causal link between genetically predicted CTSD levels and BC risk. Single-cell analysis showed CTSD specifically enriched in myeloid cells; CTSD⁺ myeloid cells displayed immunosuppressive signatures and therapy resistance. CTSD⁺ epithelial cells interacted with cancer-associated fibroblasts via FGF signaling and showed altered metabolism. GraphBan predicted and experiments confirmed Aurantio-obtusin as a high-affinity CTSD inhibitor. Molecular simulations demonstrated stable binding of both PFAS and Aurantio-obtusin to CTSD. Histologically, elevated CTSD expression co-localized with CD68⁺ macrophages in PNI-positive TNBC tissues, while Aurantio-obtusin suppressed CTSD expression and inhibited TNBC cell proliferation and migration. This study suggests that PFAS exposure is associated with PNI and malignant progression in TNBC, potentially involving dysregulation of CTSD. The robust PPG-based prognostic signature and the natural inhibitor Aurantio-obtusin offer novel biomarkers and a potential therapeutic strategy for mitigating PFAS-related cancer risks. - Source: PubMed
Publication date: 2026/05/20
Chen ShuranSu RongshengYin ZhenglangChen HaohaoLiu YanyanLi Angqing - The hemolysin co-regulator protein (Hcp) is a core virulence protein of the Type VI Secretion System (T6SS) in avian pathogenic Escherichia coli (APEC) and plays a critical role in host-pathogen interactions. While several bacterial effectors are known to subvert host immunity by modulating autophagy, whether and how the APEC Hcp2a protein influences autophagy in chicken macrophages (HD11) remains unclear. Here, we demonstrate that Hcp2a is efficiently internalized into HD11 cells and induces significant cytotoxicity. Notably, Hcp2a treatment elicited an autophagic response, as evidenced by elevated LC3-II levels and increased formation of autophagic vesicles. However, this was accompanied by p62/SQSTM1 aggregation and impaired autophagic flux, indicating a blockade in autophagosome-lysosome degradation. Quantitative proteomic analysis revealed significant down-regulation of the lysosomal pathway, particularly of key components involved in acidification and proteolysis. Functional assays confirmed that Hcp2a causes lysosomal dysfunction, characterized by the reduction in acidic lysosomal compartments and decreased levels of mature cathepsin D (CTSD). These defects ultimately impair the degradative capacity of lysosomes following autophagosome fusion, culminating in the block of autophagic flux. Our findings uncover a mechanism by which APEC Hcp2a interrupts host autophagy through lysosomal impairment, providing novel insights into APEC pathogenesis and bacterial immune evasion strategies. - Source: PubMed
Publication date: 2026/04/28
Tian YaqinZhang YuqiLu LitingWang ShuhuiDai LiyangWang HaiyangNawaz SaqibSun JiumengShao YingWang ZhengyuTu JianSong Xiangjun - C3a-driven macrophage-myofibroblast transition (MMT) is a key pro-fibrotic event after acute skeletal muscle injury, with no effective treatment available. Quercetin is a bioactive flavonoid with anti-inflammation potential; however, its impact on muscle fibrosis remains unclear. - Source: PubMed
Publication date: 2026/05/12
Li YuqiQi BeijieLuo ZhiwenChen JiwuFang ChaohuaSun Yaying