Ask about this productRelated genes to: TIMP3 antibody
- 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 antibody
Related articles to: TIMP3 antibody
- Hepatocellular carcinoma (HCC) is a crucial health concern worldwide, representing a leading cause of cancer-related mortality and the most common form of primary liver cancer. The aggressive nature of HCC is mainly due to its high tendency for invasion and metastasis, processes regulated by a complex network of genetic and molecular pathways. Among the critical regulators of these processes is microRNA-21 (miR-21), a small non-coding RNA that implicated in various oncogenic activities. This review provides a comprehensive analysis of the role of miR-21 in promoting HCC metastasis, with a particular focus on its interaction with key signaling pathways, including the PTEN/PI3K/AKT, PDCD4/AP-1, RECK/MMP, and TIMP-3 axes. By targeting tumor suppressors, miR-21 facilitates epithelial-to-mesenchymal transition (EMT), invasion, and metastasis of HCC cells. Understanding the molecular mechanisms regulated by miR-21 not only sheds light on the pathogenesis of HCC but also highlights potential therapeutic targets for combating this aggressive cancer. - Source: PubMed
Alaee MahdiMoulaee MeysamTaebi KimiaHaghi AhouraHormozi MaryamAzad Mehdi - Fibro/adipogenic progenitors (FAPs) are multipotent stromal cells that support myofiber regeneration, but can also give rise to intramuscular adipose tissue (IMAT) and fibrotic scar tissue. While the Hedgehog pathway suppresses FAP adipogenesis and promotes myofiber repair through ligand Desert Hedgehog, the key cell type that senses this signal has remained unclear. Here, we demonstrate through FAP-specific deletion of the Hedgehog signal transducer Smoothened that FAPs are the primary Hedgehog-responding cells during muscle regeneration. Loss of Smoothened in FAPs increases IMAT, causes persistent fibrosis, reduces the Hedgehog-dependent effectors TIMP3 and GDF10, and impairs myofiber regeneration. FAPs lacking Smoothened also fail to support myoblast differentiation and fusion as efficiently as control FAPs, showing that Hedgehog signaling helps establish a pro-myogenic FAP state early after injury. Pharmacological Hedgehog activation via the Smoothened agonist SAG fails to rescue adipocyte accumulation or myofiber regeneration when FAPs lack Smoothened. Together, these findings provide direct genetic evidence that FAPs are the primary cellular mediators of Hedgehog signaling in muscle and establish FAP Hedgehog signaling competence as a key determinant of regenerative outcome and a target for restoring muscle repair in disease. - Source: PubMed
Publication date: 2026/06/02
Liu XinyueHe VincentDeepesh BenedictNorris AlessandraKopinke Daniel - This study investigates the combined therapeutic effects of myricetin (Myr) and quercetin (Que) on miRNA-140 regulation and the MMP/TIMP signaling pathway involved in cartilage matrix remodeling in osteoarthritis (OA). - Source: PubMed
Bai HongzhuXu YanhuaZhao BagennaQin XiongMeng JianjunHan ZhendongCha SunaJin Gang - BackgroundVarious studies have reported altered expression of metalloproteinases in Alzheimer's disease (AD); however, expression profiles of each metalloproteinase during cognitive decline have not yet been fully characterized.ObjectiveThe purpose of this systematic review was to generate a comprehensive overview of metalloproteinases and their cognate inhibitors expression in AD and mild cognitive impairment (MCI), across sample matrices, to determine whether metalloproteinases are dysregulated in AD and may have predictive power in individuals with cognitive decline.MethodsAn electronic literature search was conducted in PubMed, EMBASE, Scopus and MEDLINE from inception to December 2024. Sixty-one publications reporting metalloproteinase and inhibitor levels in 8576 patients with AD or MCI, and 7333 controls were included in the systematic review, twenty-one of which were extracted for meta-analysis. Standardized mean difference (SMD) was used to illustrate comparisons, and the Newcastle-Ottawa scale to assess bias.ResultsHigher levels of cerebrospinal fluid (CSF) tissue inhibitor of metalloproteinase-2 (TIMP-2; = 0.0003) were observed in the AD group and in patients with MCI ( = 0.0009) compared to cognitively healthy controls. Following sensitivity analysis, significantly higher levels of CSF MMP-10 ( = 0.0005) and lower plasma TIMP-2 ( = 0.004) were also noted in patients with AD. TIMP-3, across all sample matrices, was decreased in patients with MCI versus controls ( = 0.01).ConclusionsSignificantly altered levels of metalloproteinases and their inhibitors were verified between patients with AD and MCI, representing potential biomarkers and prospective therapeutic targets for cognitive decline. This study was registered with PROSPERO, CRD42024628202. - Source: PubMed
Publication date: 2026/06/06
McNaugher GillianMcColgan LeahChurch MiaMcClean Paula LGibson David SMurray Elaine KCoyle SophieMcGilligan Victoria - Surgical repair of rotator cuff injuries is frequently complicated by high retear rates, driven by persistent inflammation and inadequate tissue regeneration. Exosomes derived from M2 macrophages represent a promising therapeutic avenue due to their innate immunomodulatory and regenerative properties. However, their clinical application is hindered by low yields and complex purification processes. In this study, we employed an extrusion technique to isolate exosome mimetics from platelet-rich plasma (PRP) pretreated M2 macrophages. These engineered vesicles, termed PRP-M2-EM, acquired additional bioactive factors from PRP, which significantly enhanced their pro-angiogenic and immunoregulatory functions compared to standard M2-EM. This biomimetic engineering strategy successfully transposes the therapeutic benefits of PRP into a stable, nanoscale delivery system, overcoming the limitations of PRP's short half-life and high production costs. Mechanistically, we identified the enrichment of miR-21a-5p within PRP-M2-EM as a primary driver of their superior efficacy. Further mechanistic investigation revealed that the high expression of miR-21a-5p in PRP-M2-EM targets and inhibits the tissue inhibitor of metalloproteinase 3 (TIMP3) gene, facilitating a regenerative environment. In conclusion, our study introduces engineered PRP-M2-EM as a potential therapeutic strategy. This approach promotes rotator cuff regeneration through enhanced angiogenesis and immunomodulation, with the miR-21a-5p/TIMP3 axis potentially contributing to these effects. - Source: PubMed
Publication date: 2026/06/02
Lin ChihaoJiang HongyiChen LinjieZhu LiangWang YuhanShen HantingLin ZhongnanShi JunfengWang JilongDeng JunjiePan Xiaoyun