TIMP2 _ TIMP_2 Protein (Native)
- Known as:
- TIMP2 _ TIMP_2 Protein (Native)
- Catalog number:
- 10396-HNAH
- Product Quantity:
- 50
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- TIMP2 _ TIMP_2 Protein (Native)
Ask about this productRelated genes to: TIMP2 _ TIMP_2 Protein (Native)
- Gene:
- TIMP2 NIH gene
- Name:
- TIMP metallopeptidase inhibitor 2
- Previous symbol:
- -
- Synonyms:
- CSC-21K
- Chromosome:
- 17q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-06-18
- Date modifiied:
- 2016-10-05
Related products to: TIMP2 _ TIMP_2 Protein (Native)
Related articles to: TIMP2 _ TIMP_2 Protein (Native)
- Pediatric acute kidney injury (AKI) often presents insidiously and progresses rapidly. Traditional diagnostic criteria based on serum creatinine and urine output are markedly delayed and insufficient to capture injury patterns across different etiologies. This paper aims to summarize recent advances in pediatric AKI biomarker research since the release of the ADQI 23 (2020) consensus. Focusing on three major clinical scenarios-cardiac surgery, sepsis, and nephrotoxic drugs-it reviews early biomarker evidence and explores their potential applications in risk stratification. At the mechanistic level, this paper outlines key pathological pathways in pediatric AKI progression: oxygenation-perfusion imbalance after cardiac surgery, endothelium-immune dysregulation driven by sepsis, and tubular-mitochondrial injury associated with nephrotoxic exposure. In CS-AKI, uNGAL shows the earliest elevation within hours after cardiopulmonary bypass, followed by sequential changes in IL-18, L-FABP, and KIM-1. [TIMP-2] × [IGFBP7] and exosomal miRNA aid in identifying high-risk or severe AKI. In SA-AKI, suPAR and glycocalyx/endothelial injury markers (e.g., syndecan-1, Angpt-2/sTM/Tie-2), combined with urinary DKK3 and complement Ba, can be used for early risk stratification and predicting poor outcomes. In NT-AKI, uNGAL has high negative predictive value for excluding severe AKI, while uKIM-1, uCysC, uOPN, and multi-biomarker combinations can indicate subclinical tubular injury earlier after drug exposure. Overall, single biomarkers struggle to cover AKI heterogeneity. Future efforts should integrate functional dynamic assessments (e.g., FST, RRI), scenario-based multi-biomarker combinations, and AI dynamic models to propose evidence-based, scenario-stratified identification pathways. These will serve as structured references for prospective studies and clinical workflow optimization. - Source: PubMed
Publication date: 2026/05/06
Jin WenqinYe QingCheng Dongqing - Acute kidney injury (AKI) is a life-threatening condition whose early diagnosis is crucial. The most used method to evaluate renal function is the glomerular filtration rate (eGFR). The detection of new circulating molecules has gained traction for the early identification of kidney damage. In this prospective observational study, 57 patients with acute kidney disease and 23 patients without acute renal damage were consecutively enrolled; urinary concentrations of NGAL, LFABP, CYR61, TIMP-2, IGFBP-7, and [TIMP-2 X IGFBP-7], and serum concentrations of PENK and KIM-1 were obtained in all patients. The primary endpoint was to assess the role of serum and urinary markers in distinguishing prerenal from renal pathogenesis of AKI. The secondary endpoint was to evaluate the possible association between urinary and serum concentrations of these markers and the severity of acute kidney injury. Urinary TIMP-2, NGAL, and IGFBP-7 concentrations were higher in patients with AKI compared with the control group, with statistical significance. Among patients with AKI, we found higher concentrations of LFABP, Cyr61, TIMP-2, NGAL, IGFBP-7, and [TIMP-2]x[IGFBP-7] according to AKI aetiology, with statistical significance maintained in multivariable logistic regression for IGFBP-7. The ROC curve confirmed that IGFBP-7 has a predictive role in the aetiological diagnosis of AKI. A significant association between urinary LFABP and TIMP-2 and serum KIM-1 concentrations (p = 0.0001) and the variation in creatinine values from baseline to enrollment was found. Furthermore, we found a statistically significant correlation between KIM-1 and the variation in creatinine levels from admission to discharge. This study highlights an association between the concentrations of the novel biomarkers and the aetiology of AKI, with a possible role for these molecules in stratifying patients with acute renal disease. - Source: PubMed
Publication date: 2026/05/04
Pacinella GaetanoBasso Maria GraziaMiceli GiuseppeCasuccio AlessandraDaidone MarioScaglione StefaniaTodaro FedericaPintus ChiaraRizzo GiulianaTuttolomondo Antonino - Diabetic cardiomyopathy (DCM) features progressive fibrotic remodeling, but the shared molecular circuitry connecting diabetes mellitus (DM) to cardiomyopathy (CM) remains unclear. We integrated three DM- and three CM-related Gene Expression Omnibus (GEO) datasets and corrected batch effects with sva, verified by violin plots, principal component analysis (PCA), and silhouette coefficients computed on all common genes (DM: 0.9489 to -0.1016; CM: 0.9693 to -0.045; PC1/PC2 inter-batch differences abolished after normalization). Differential expression analysis identified 2562 DM Differentially expressed genes (DEGs) and 1414 CM DEGs, and their intersection yielded 91 common DEGs (51 upregulated, 40 downregulated). Protein-protein interaction (PPI) analysis prioritized 25 hub genes, whose enrichment profiles implicated insulin resistance/insulin signaling and adrenergic signaling in cardiomyocytes. TRRUST-based inference further defined a regulatory network centered on seven key genes (, , , , , , and ). To nominate a candidate target of oxymatrine (OMT), we performed docking and molecular dynamics (MD) simulations for representative complexes; OMT showed the most stable interaction with LTBP1, maintaining a consistently short pocket distance (~0.2 nm), the highest contact frequency, and the lowest MM/PBSA binding free energy (-15.32 kcal/mol), with favorable contributions dominated by van der Waals and nonpolar solvation terms. In primary cardiac fibroblasts (CFs), high glucose (HG, 30 mM glucose) induced proliferative and profibrotic activation, whereas OMT (0.4-0.8 mM) reduced HG-driven proliferation without detectable toxicity below 1.2 mM, suppressed FN, collagen I/III, and α-SMA expression, and inhibited migration. OMT also normalized HG-induced cell-cycle skewing by restoring G0/G1-phase occupancy and reducing S-phase entry, with effects comparable to metformin. Finally, HG increased LTBP1 expression and upregulated SMAD3/SMAD4, while OMT attenuated LTBP1 induction and suppressed downstream TGF-β/SMAD activation. Together, these data integrate cross-dataset transcriptomics with mechanistic validation to position LTBP1 as a putative antifibrotic node targeted by OMT, supporting inhibition of the LTBP1/TGF-β/SMAD axis as a candidate strategy to counter DCM-associated fibrosis. - Source: PubMed
Publication date: 2026/04/13
Tian LianqingGan ShiquanDu YouqiLong ChaowenChang ChuruiShen Xiangchun - Graphene oxide (GO) is a promising nanocarrier for the delivery of oligonucleotides. It offers a high loading capacity, efficient cellular uptake, and surface functionalization. MicroRNA-21 (miR-21) is a well-characterized oncomiR commonly overexpressed in hepatocellular carcinoma (HCC). In HCC, miR-21 contributes to tumor progression, inflammation, and angiogenesis. In a previous in vitro study, we showed that GO alone induces the upregulation of pro-inflammatory and tumor-related genes in HepG2 cells. However, conjugation with an antisense miR-21 (GO-antisense miRNA 21) reverses this effect, suggesting a potential therapeutic application. This study aims to evaluate the antitumor and anti-angiogenic efficacy of the GO-antisense miR-21 nanosystem using the chick embryo chorioallantoic membrane (CAM) model. Fertilized chicken eggs ( = 4 per group) were randomized into untreated, GO-treated, and GO-antisense miR-21-treated cohorts. A dose of 200 μL (GO 10.0 µg/mL: antisense miR-21 5.0 pmol/mL) was administered intratumorally. Tumor size, volume, and vascularization were monitored through stereomicroscopy and histological analysis. The expression of inflammatory and tumor-associated genes (IL-8, MCP-1, TIMP-2, ICAM-1 and NF-kB) was assessed by quantitative PCR. Given its prominent response, IL-8 protein expression was further analyzed via immunofluorescence. To evaluate tumor-specific delivery, FITC-labeled GO was tracked by confocal microscopy. Our data revealed that treatment with unfunctionalized graphene oxide (GO) unexpectedly promoted tumor vascularization and led to a significant increase in tumor weight. This was accompanied by upregulation of inflammatory markers. In contrast, GO-antisense miR-21 significantly reduced the tumor volume and vessel density. It also successfully downregulated all target genes. Confocal imaging demonstrated preferential accumulation of the nanosystem within the tumor mass. Our results highlight the dual anti-inflammatory and anti-angiogenic effects of GO-antisense miRNA 21 and support its potential as a targeted nanoplatform for HCC treatment. - Source: PubMed
Publication date: 2026/04/01
Trischitta PaolaNasiłowska BarbaraPennisi RosamariaCosta MariannaSciortino Maria TeresaKutwin Marta - Diabetic retinopathy (DR) is a common comorbidity of diabetes involving the formation of abnormal vascular structures in the retina. Tissue inhibitor of metalloproteinases 2 (TIMP2), initially identified as a key mediator of extracellular matrix turnover, is pivotal for inflammatory processes and tissue homeostasis. The current study examined the influence of gene variations on the risk for DR. - Source: PubMed
Huang Chin-TeChien Hsiang-WenWang KaiSu Shih-ChiTing Chin-HanYang Shun-FaLiao Miao-Yu