Ask about this productRelated genes to: TIMP3 Blocking Peptide
- Gene:
- TIMP3 NIH gene
- Name:
- TIMP metallopeptidase inhibitor 3
- Previous symbol:
- SFD
- Synonyms:
- -
- Chromosome:
- 22q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 1993-04-12
- Date modifiied:
- 2014-11-19
Related products to: TIMP3 Blocking Peptide
Related articles to: TIMP3 Blocking Peptide
- Gliomas, particularly glioblastoma, remain difficult to control because diffuse infiltration into surrounding brain tissue limits complete resection and contributes to recurrence. Cannabidiol (CBD), a nonpsychoactive cannabinoid capable of entering the central nervous system, has shown antitumor activity in glioma models, but the mechanisms underlying its anti-invasive effects remain unclear. Lysyl oxidase-like 2 (LOXL2) regulates extracellular-matrix remodeling and mesenchymal phenotypes in several cancers. We therefore tested the hypothesis that CBD limits glioma growth and invasion partly by suppressing an LOXL2-associated extracellular-matrix and EMT-like program. - Source: PubMed
Guan LeiDeng XuyanZheng JingYang ZejiJiang XiaoxiaWang Yan - This study aims to systematically elucidate the shared and specific genetic basis of osteoarthritis (OA) and obesity by integrating large-scale genome-wide association study (GWAS) summary statistics, cross-tissue quantitative trait loci (QTLs), and single-cell and spatial transcriptomic data. - Source: PubMed
Publication date: 2026/08/13
Lin ZehongWei JihuZhou Honghai - Vitamin D has been reported to act as a tissue-protective regulator by suppressing Matrix Metalloproteinases (MMPs) and upregulating Tissue Inhibitors of Metalloproteinases (TIMPs), though changes may be body mass index (BMI)-dependent; however, the relationship between vitamin D metabolism and matrix remodeling pathways in Polyendocrine Metabolic Ovarian Syndrome (PMOS) remains poorly understood. In women with PMOS ( = 28) and controls ( = 28), 12 MMPs and 3 TIMPs were determined by Slow Off-rate Modified Aptamer (SOMA)-scan plasma protein measurement and correlated to 25-hydroxyvitamin D (25(OH)D) and its metabolites (active 1,25-dihydroxyvitamin D (1,25(OH)D) and 24,25-dihydroxyvitamin D (24,25(OH)D)) measured by gold standard isotope-dilution liquid chromatography tandem mass spectrometry. Insulin resistance and systemic inflammation (normal C-reactive protein) were comparable between PMOS and control women, though PMOS had higher free androgen index and anti-Mullerian hormone levels. Vitamin D and its metabolites did not differ between groups. Only MMP16 was lower in PMOS than controls (549.6 ± 58.3 vs. 678.0 ± 304.1 Relative Fluorescent Units, = 0.037) but did not pass the false discovery rate. In women with PMOS, 25(OH)D and 24,25(OH)D demonstrated significant inverse correlations with TIMP3 (r = -0.60, = 0.005 and r = -0.58, = 0.007, respectively). Multivariable regression confirmed independent inverse associations between TIMP3 and both 25(OH)D (β = -51.1, = 0.031) and 24,25(OH)D (β = -858.7, = 0.028) after adjustment for age, body mass index and Homeostatic Model Assessment-Insulin Resistance, and the association remained stable following bootstrap internal validation. Additional moderate associations were observed between vitamin D metabolites and membrane-type MMPs (MMP14, MMP16, MMP17). Exploratory analyses suggested potential inverse associations between vitamin D metabolites and TIMP3, together with weaker associations involving MMP14, MMP16 and MMP17, suggesting the novel hypothesis that vitamin D may influence extracellular matrix remodeling and ovarian stromal biology through regulation of TIMP3-dependent pathways independently of obesity and insulin resistance, rather than through MMPs directly. - Source: PubMed
Publication date: 2026/07/24
Zainalabedin MashaelSmahi NoraSathyapalan ThozhukatButler Alexandra EAtkin Stephen L - Inflammatory myofibroblastic tumor (IMT) is a rare mesenchymal neoplasm characterized by myofibroblastic spindle cells and inflammatory infiltrates. - Source: PubMed
Publication date: 2026/08/10
Reithofer MarlenePesto LejlaHütten TobiasJurejevcic AnjaRößmann-Tsybrovskyy MartinaTervonen HannaleenaThurnher Dietmar - Osimertinib resistance limits EGFR-mutant non-small cell lung cancer (NSCLC) treatment efficacy. Cancer-associated fibroblasts (CAFs), tissue inhibitor of metalloproteinases 3 (TIMP3), and matrix metalloproteinase 9 (MMP9) are involved in resistance. Fuzheng Sanjie Formula (FZSJF) is used clinically, but its mechanism is unclear. - Source: PubMed
Publication date: 2026/08/04
Wang YifanPeng QinZhang YuannaWang HaozhuZhu JingwenZhou Jihong