Ask about this productRelated genes to: TIMP1 antibody
- 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 antibody
Related articles to: TIMP1 antibody
- Liver inflammation and fibrosis are directly associated with non-alcoholic fatty liver disease (NAFLD). Dysregulation of the potent pro-inflammatory cytokine interleukin-1 beta (IL-1β), inducible nitric oxide synthase (iNOS), and tissue leukocyte infiltration (CD45 +ve) are connected with multiorgan injury and fibrosis. We investigated whether the induction of NAFLD can cause dysregulation in the hepatic IL-1β/iNOS and IL-1β/CD45 axes of inflammation and fibrosis, as well as in endogenous metabolites (lipids, glucose, and insulin) and apoptosis, in the presence and absence of the flavonoid quercetin. - Source: PubMed
Publication date: 2026/04/21
Alqahtani Saif AAlshehri Hanan HAshour HendAbdallah HendRashed LailaBadi Rehab MMohammed Muataz E DAl-Ani BahjatAlzamil Norah MAlbawardi AliaAboulhoda Basma E - Stanford type A aortic dissection (TAAD) is a life-threatening cardiovascular condition associated with high mortality. Ferroptosis has been implicated in TAAD pathogenesis, but comprehensive analyses and experimental validation of ferroptosis-related driver genes (FRDGs) remain limited. This study systematically investigated FRDGs in TAAD using bioinformatics and experimental approaches. Differentially expressed ferroptosis-related driver genes (DEFRDGs) were identified by integrating the GSE153434 dataset with the FerrDb database. Functional enrichment analysis was subsequently performed, followed by the construction of a protein-protein interaction (PPI) network, assessment of immune cell infiltration, and prediction of potential miRNA interactions. Candidate hub genes were then validated using an independent cohort (GSE52093) and clinical tissue samples, with their diagnostic value evaluated via receiver operating characteristic (ROC) curve analysis and their protein expression confirmed by immunohistochemistry. We identified 25 DEFRDGs (17 upregulated, 8 downregulated) enriched in oxidative stress, iron binding, and ferroptosis/HIF-1 signaling pathways. Six hub genes (HIF1A, IL6, TIMP1, SAT1, HMOX1, LPCAT3) were significantly upregulated in validation cohorts, five genes (HIF1A, TIMP1, SAT1, HMOX1, LPCAT3) achieved an area under the curve (AUC) of 1.000, while IL6 also exhibited high diagnostic accuracy (AUC = 0.914). Fibroblast infiltration was elevated in TAAD tissues. Further miRNA interaction prediction revealed the potential involvement of miRNAs, such as miR-138-5p, miR-18b-5p, miR-199a-5p, miR-185-5p, miR-506-3p and miR-4644. Immunohistochemistry confirmed increased protein expression of HIF1A, SAT1, and LPCAT3. These three genes emerge as key ferroptosis-related drivers in TAAD. Their consistent upregulation and strong diagnostic performance support ferroptosis as a potential therapeutic target and provide a basis for mechanism-focused interventions. - Source: PubMed
Publication date: 2026/04/07
Nie RuizhiHan WeiqingXu Jianjun - Tissue remodeling critically depends on fibroblasts and macrophages, but the timely and coordinated induction of phenotypes that promote remodeling-associated extracellular matrix (ECM) and interstitial collagen degradation is poorly understood. Here, we exploit the potency of activated dermal fibroblasts and macrophage plasticity to study cell-cell interplay. We identify fibroblasts as vigorous stimulators of co-cultured macrophages' differentiation towards a collagen-clearing phenotype. Fibroblasts secrete several soluble factors with macrophage recruitment and stimulation potential, including M-CSF, CXCL-1, CCL2, IL-6, and TIMP-1. IL-6-driven upregulation of Mannose Receptor (MR, CD206), an endocytic collagen-clearance receptor, is identified as a key macrophage effector-response. Mouse dermal in situ collagen turnover models demonstrate that macrophage MR-dependent collagen-uptake constitutes a recruitable pathway that can readily facilitate collagen degradation and links IL-6 macrophage-stimulation to the process. Importantly, a novel fibroblast depleter system reveals that fibroblasts dictate macrophage differentiation and collagen-clearance in vivo. Our study establishes activated fibroblasts as critical orchestrators of macrophage functions with potential impact on physiological tissue remodeling and fibrosis. - Source: PubMed
Publication date: 2026/04/24
Heltberg Signe Spliidvan Putten SanderKrigslund OliverNørregaard Kirstine SandalIpsen David HøjlandBehrendt NielsEngelholm Lars HenningJürgensen Henrik Jessen - Bothrops envenomation induces extensive local tissue destruction and a robust inflammatory response, largely driven by the host's endogenous molecular pathways. Among these, Matrix Metalloproteinases (MMPs), zinc-dependent endopeptidases responsible for extracellular matrix (ECM) degradation, play a central role. The clinical severity of envenomation is therefore strongly influenced by the balance between MMPs and their specific inhibitors, the TIMPs. This study investigated the contribution of MMP-1, MMP-2, MMP-7, MMP-9, and MMP-10 and TIMP-1, TIMP-2, TIMP-3, and TIMP-4 to the inflammatory response following Bothrops snakebites. - Source: PubMed
Publication date: 2026/04/24
Ferreira Neves Juliana CostaMagalhães-Gama FábioSantos Ibiapina Hiochelson NajibeSeixas Kamille BeltrãoBarbosa Êndila SouzaMalheiro AdrianaGonçalves Sachett Jacqueline AlmeidaCampi-Azevedo Ana CarolinaMartins-Filho Olindo AssisTeixeira-Carvalho AndréaSartim Marco AurélioMonteiro WueltonCosta Allyson Guimarães - Traumatic brain injuries (TBIs) are a common cause of morbidity and mortality after major trauma. In addition to local injury effects, TBI is associated with a systemic inflammatory response and acute lung injury (ALI), which increases mortality and worsens neurological outcomes. The exact mechanism of this ALI is not known. Extracellular vesicles (EVs) are small cell-derived particles involved in cell-cell communication that carry a wide variety of payloads, including proteins and microRNAs (miRNAs), which can mediate inflammation. We sought to characterize EV-derived miRNAs associated with TBI-induced ALI. - Source: PubMed
Publication date: 2026/04/24
Johnston WilliamArzave JulissaYuengert ConnorPark Dong JunCostantini Todd WEliceiri Brian PWeaver Jessica L