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
- This study aimed to determine whether hepatocytes acquire stemness properties during their dedifferentiation toward myofibroblast-like phenotype and to evaluate the role of TGF-β1 signaling in mediating this process during liver fibrosis (LF) progression. LF was induced in male Sprague-Dawley (SD) rats, and tissues were analyzed at 4, 8, and 12 weeks using histological staining, immunohistochemistry, immunofluorescence, and biochemical approaches. In parallel, in-vitro experiments were performed in HepG2 cells to further investigate fibrosis-related signaling mechanisms. TA administration resulted in progressive hepatocellular injury, characterized by macrophage infiltration/inflammation and extensive collagen deposition in the periportal and central vein areas. Persistent oxidative stress was evidenced by increased NOX2 and malondialdehyde (MDA) levels, together with reduced antioxidant defenses. These alterations were associated with sustained activation of the Smad2/Smad3 pathway downstream of TGF-β1. Concurrently, hepatocytes showed induction of stemness-associated transcription factors, including Oct4, Runx2, and Sox9, along with partial loss of hepatocyte identity markers such as albumin and HNF4α, suggesting the acquisition of partial myofibroblast-like characteristics, including α-SMA and Col I and Col III expression. Dysregulated extracellular matrix turnover was further indicated by increased TIMP1 and reduced MMP9 expression. In-vitro inhibition of TGF-β1 signaling and suppression of Oct4 significantly attenuated TA-induced fibrotic responses in HepG2 cells, supporting the role of TGF-β1-Oct4 signaling in hepatocyte partial differentiation and LF remodeling. This dual mechanism underscores the role of hepatocyte differentiation in LF progression and broadens the therapeutic landscape. - Source: PubMed
Publication date: 2026/05/01
Yadav ManishaVerma ShobhitVerma SmritiNerurkar RutujaKumar NandiniMudedla Sathish KumarMugale Madhav Nilakanth - Several biomarkers have been assessed for the diagnosis of chronic kidney disease (CKD). However, limited data are available regarding their ability to predict mortality in CKD. The aim of this study was to assess the ability of lipocalin-2, receptor for advanced glycation end products (RAGE), tissue inhibitor of metalloproteinase 1 (TIMP-1), osteopontin, and trefoil factor 3 (TFF-3) in predicting the prognosis of patients with CKD. - Source: PubMed
Publication date: 2026/01/19
Padmanabhan RaghavanManoharan KaviyaSahay MelinaBhujangarao PoojaGoenka LuxitaaPriya SolaiSubramaniyan KumarasamySriram Damal KandadaiGeorge Melvin - Progressive fibrosis is a hallmark of Duchenne muscular dystrophy (DMD) pathology, driving muscle degeneration and failure. However, the key transcriptomic programs and hub gene networks associated with extracellular matrix remodeling in DMD remain incompletely characterized. We employed weighted gene coexpression network analysis (WGCNA) on transcriptomic data to identify disease-associated modules. Through intersection with GeneCards and topological screening of protein-protein interaction networks, key hub genes were isolated. We further characterized the immune microenvironment via CIBERSORT and traced the cellular origin of the signature using single-cell RNA sequencing (scRNA-seq). Finally, drug prediction coupled with molecular docking was validated in vitro using a TNF-induced fibroblast inflammation model. Six pivotal hub genes (COL1A1, COL1A2, COL3A1, DCN, SPARC, and TIMP1) were identified, all exhibiting significant upregulation and exceptional diagnostic value (AUC > 0.90). This signature was intimately linked to a proinflammatory microenvironment dominated by macrophages and γδ T cells. Crucially, scRNA-seq mapped these fibrotic signals specifically to tendon fibroblasts. Halofuginone was identified as a candidate therapeutic agent, showing robust binding affinities (< - 5.0 kcal/mol) to the hub proteins. In vitro assays showed that halofuginone significantly reduced the mRNA and protein abundance of these fibrosis-associated hub genes under inflammatory stimulation. This study delineates a tendon fibroblast-derived gene signature associated with DMD fibrosis and provides supportive evidence that halofuginone may modulate this hub network, highlighting its potential as an antifibrotic candidate in DMD. - Source: PubMed
Publication date: 2026/04/29
Luo ZhiliHu FangWei XiaolingChen MinWang Xiaolin - Stress urinary incontinence (SUI) is one of the most prevalent pelvic floor disorders in women, and it is pathologically linked to collagen metabolism imbalance. Current treatments face limitations, including suboptimal efficacy and invasiveness. radiofrequency therapy (RF) therapy has emerged as a promising non-invasive approach, yet its precise mechanisms, particularly concerning collagen remodeling, remain inadequately elucidated.This study aimed to investigate the effects of RF on vaginal collagen metabolism in SUI rats and elucidate its underlying molecular mechanisms. An SUI rat model was created via vaginal dilation and bilateral ovariectomy. Rats were divided into Sham, SUI, SUI-No-RF, and SUI-RF ( = 7/group). The SUI-RF group received RF treatment (500 kHz, 2 W, 40 °C–42 °C) every 5 days for 3 sessions. At week 3 post-modeling, urodynamic measurements, Masson’s trichrome staining, immunofluorescence, Transmission Electron Microscopy (TEM), Western blot, and quantitative real-time polymerase chain reaction ( qPCR) were performed. Compared to the Sham group, SUI rats exhibited significantly reduced bladder leak point pressure (BLPP) and abdominal leak point pressure (ALPP) ( < 0.001). RF treatment markedly increased BLPP and ALPP in the SUI-RF group versus SUI-No-RF ( < 0.001), restoring urinary continence. Vaginal tissue in the SUI-RF group exhibited collagen volume fraction, elevated type III Collagen expression, and restored fibril alignment ( < 0.05). Mechanistically, RF treatment activated the Transforming Growth Factor-β1 (TGF-β1)/Smad2 pathway (increased TGF-β1 expression and Smad2 phosphorylation), upregulated tissue inhibitor of metalloproteinase 1 (TIMP1), and suppressed matrix metalloproteinase 9 (MMP9) expression ( < 0.05). RF therapy restores vaginal collagen architecture and continence function in SUI rats by activating the TGF-β1/Smad2 pathway and bidirectionally modulating the MMP9/TIMP1 equilibrium. These findings elucidate a molecular mechanism for RF therapy and support its further development as a non-invasive treatment for SUI. - Source: PubMed
Publication date: 2026/04/29
Zhu LipingZhou YanhuaTong YaoZhou ChengyuJiang LiLi Xuhong - Yiqi Jianpi Decoction (YJD) is a traditional Chinese medicinal formula with reported anticancer properties; however, its effects and regulatory mechanisms in colorectal cancer (CRC) are unclear. Active components and their targets in YJD were identified via the Traditional Chinese Medicine Systems Pharmacology (TCMSP) platform, and differentially expressed genes in CRC were extracted from The Cancer Genome Atlas to define the drug-target genes. Potential mechanisms of YJD in CRC were explored through protein-protein interaction network and GO/KEGG enrichment analyses. An cell model was established: Transwell invasion, wound-healing, and flow-cytometry assays were used to monitor CRC cell viability, while carboxifluorescein diacetate succinimidyl ester assay and lactate dehydrogenase release assay assessed CD8 T-cell activation. TCMSP screening results showed that the compound Nobiletin (NOB) in YJD interacted with the CRC-related gene TIMP1. experiments demonstrated that TIMP1 expression levels were positively correlated with CD274 and dampened the cytotoxic effect of CD8 T cells against CRC. NOB, by binding to TIMP1, inhibited CD274 expression, enhanced CD8 T-cell activity and proliferation, and thereby boosted their cytotoxic effects on CRC cells. The compound NOB in YJD can enhance the cytotoxicity of CD8 T cells against CRC by targeting the TIMP1/CD274 axis. - Source: PubMed
Publication date: 2026/04/29
Luo LanZhou FangLiu Zheng