Ask about this productRelated genes to: TIMP1 protein
- Gene:
- TIMP1 NIH gene
- Name:
- TIMP metallopeptidase inhibitor 1
- Previous symbol:
- TIMP, CLGI
- Synonyms:
- EPO
- Chromosome:
- Xp11.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2017-07-26
Related products to: TIMP1 protein
Related articles to: TIMP1 protein
- Matrix metalloproteinases (MMPs) are a family of proteases that drive degradation of extracellular matrix (ECM) across many tissues. MMP activity is antagonized by tissue inhibitors of metalloproteinases (TIMPs), resulting in a complex multivariate system with many MMP isoforms and TIMP isoforms interacting across a network of biochemical reactions - each with their own distinct kinetic rates. This system complexity makes it very difficult to identify which specific molecules are most responsible for driving ECM turnover in vivo and therefore the most promising therapeutic targets. To help elucidate the specific roles of various MMP and TIMP isoforms, we present a computational systems biology model of collagen turnover capturing all possible interactions between type I collagen, four different MMP isoforms (MMP-1, -2, -8, and -9), and three different TIMP isoforms (TIMP-1, -2, and -4). We used dye-quenched fluorescent collagen to monitor the degradation of collagen in the presence of various MMP + TIMP cocktails, and we then used these experimental data to fit hypothetical reaction system topologies in order to investigate their respective accuracies. We determined kinetic rate constants for this system and used post-myocardial infarct time courses of collagen, MMP, and TIMP levels to perform a parameter sensitivity analysis across the model reaction rates and predict which molecules and interactions are the important regulators of ECM in the infarcted heart. Notably, the model suggested that MMP degradation and inactivation terms were more important for driving collagen levels than TIMP interaction terms. In sum, this work highlights the need for systems-level analyses to distinguish the roles of various biomolecules operating with a complex system, prioritizes therapeutic targets for post-infarct cardiac remodeling, and presents a computational framework that can be applied to many other collagen-rich tissues. - Source: PubMed
Publication date: 2026/08/12
Yeganegi AmirrezaRobles KarlaRichardson William J - Ferroptosis is an iron-dependent form of regulated cell death, whereas the precise mechanism of ferroptosis in the pathogenesis of ulcerative colitis (UC) remains to be elucidated. The tissue inhibitor Metalloproteinase 1 (TIMP1) is involved in ferroptosis of UC, whereas its regulatory function remains unclear. This study is aimed at exploring the potential effect on ferroptosis in UC. - Source: PubMed
Publication date: 2026/08/12
Zhou XuanQiao QiaoYang JieTu Huiming - Soft tissue sarcomas are malignant neoplasms originating from mesenchymal cells. In cats, there are two groups: inoculation site-associated sarcomas (ISSs) and non-inoculation site-associated sarcomas (NISSs). The aim of this study was to investigate the immunoexpression of metalloproteinases (MMPs) 2 and 9, tissue inhibitors (TIMPs) 1 and 2, and the main molecules related to angiogenesis and vascular count in both sarcoma groups; compare their expression; and evaluate their association with angiogenesis. Both tumor groups expressed all the molecules evaluated. A positive correlation was detected between MMP-2 and angiogenic factors in both ISSs and NISSs. MMP-9 expression correlated positively with MMP-2 in both groups. TIMP-1 correlated with both MMP and with angiogenic factors in ISS. Fibroblast growth factor receptor 2 (FGFR-2) expression was higher in NISS. Studying the pathways that regulate angiogenesis in these neoplasms is crucial for identifying ways to intervene and limit neoplastic progression, thereby developing new therapeutic approaches. - Source: PubMed
Publication date: 2026/08/06
Wright CarolinaScarano Alejo CarlosVerdes José ManuelScenna Silvana GracielaDuchene Adriana GracielaOsacar Juan ManuelDi Pierro Lucas MartínRisso PaulaBadura ErikaBarbeito Claudio GustavoAcuña FranciscoSantelices Iglesias Olga Andrea - Chronic obstructive pulmonary disease (COPD) accompanied by inflammation contributes to airway obstruction, mucus hypersecretion, and other characteristic symptoms. The airways densely innervated by subsets of nerve fibers highlight the critical role of neuroimmune interactions in disease pathogenesis. The present study aimed to investigate the role of neurogenic inflammation in COPD and evaluate the therapeutic potential of naltrexone (NTX) at ultra-low doses (10 μg/kg 1 μg/kg 0.1 μg/kg) in modulating neuroimmune signaling in cigarette smoke (CS) induced COPD. CS exposure elevated inflammatory markers (COX-2 and LOX-5), activation of the hypothalamic-pituitary-adrenal axis (increased cortisol and ACTH), and enhanced neurogenic signaling marked by increased levels of neurotransmitters (substance P, serotonin, acetylcholine, and dopamine) and upregulation of their respective receptors. Further the increased sensory ion channels (TRPV1 and TRPM8), indicating elevated neurogenic inflammation. Furthermore, COPD mice exhibited elevated fibrotic markers, including TGF-β1, α-SMA, MMP-2, and MMP-9, and TIMP-1 expression, collagen deposition, and mucus hypersecretion. NTX at low doses (0.1 μg/kg) significantly attenuated these alterations by suppressing inflammatory mediators, reducing neurogenic signaling, downregulating TRP channel expression, and mitigating fibrosis. Importantly NTX modulated both µOR and TLR4 expression, suggesting that its protective effects are mediated through coordinated regulation of the µOR-TLR4 axis, attenuating neuroimmune crosstalk. Histopathological findings confirmed restoration of lung architecture and reduction of airway remodeling. The findings suggest that neuroimmune dysregulation contributes to COPD pathology, while NTX at ultra-low-dose exerts protective effects by targeting this axis. The study further highlights the µOR-TLR4 axis as a potential therapeutic target through which NTX modulates airway inflammation and remodeling. - Source: PubMed
Publication date: 2026/08/12
Soni Sharma ShaliniSrivastava AtulChoudhary Deepak KrGaglani PratikkumarSubhashini - In clear cell renal cell carcinoma (ccRCC), mast cell activation and angiogenesis are crucial for disease progression, with interactions occurring between these processes. The involvement of mast cell-related angiogenic characteristics in ccRCC is not yet fully elucidated. To address this gap, this study aims to clarify the biological role and prognostic significance of mast cell-mediated angiogenesis in ccRCC, and to examine its links to the tumor microenvironment and disease progression. - Source: PubMed
Publication date: 2026/06/27
Ji RanDai HaojieZhang XiKong WeiyuZhang JiajunWang YangWang JiajiaTang LeyuanCao XiaoyangLiu YiyangQin Chao