Ask about this productRelated genes to: MMP13 Blocking Peptide
- Gene:
- MMP13 NIH gene
- Name:
- matrix metallopeptidase 13
- Previous symbol:
- -
- Synonyms:
- CLG3
- Chromosome:
- 11q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-11-20
- Date modifiied:
- 2016-10-05
Related products to: MMP13 Blocking Peptide
Related articles to: MMP13 Blocking Peptide
- Sebaceous gland biology depends on the integration of lipid metabolism, tissue architecture, and stromal interactions, yet most available systems fail to capture these features simultaneously. This work reports the generation of a functional three-dimensional (3D) sebaceous gland organoid embedded within a matrix and designed to reproduce the structural and functional properties of native sebaceous tissue. - Source: PubMed
Publication date: 2026/07/31
Pusceddu TommasoArdondi LunaCavaleri Maria PiaSileo LuciaVitali IlariaMeza Camila QuezadaMassironi MicheleMassironi MarcoZavan Barbara - Tongue squamous cell carcinoma (TSCC) is a highly aggressive malignancy associated with unfavorable clinical outcomes, highlighting the critical need for dependable prognostic indicators. The epithelial-mesenchymal transition (EMT) is a fundamental biological process driving cancer progression. This study aimed to develop and independently validate an EMT-associated gene expression signature for predicting prognosis in TSCC through a multi-omics strategy. - Source: PubMed
Publication date: 2026/06/24
Fu KaiLi LinWang RuyvLi JuanWang Weiyi - Non-healing wounds remain a clinical challenge due to their complex pathophysiology and limited therapeutic options. These conditions are driven by complex molecular mechanisms, including inflammation, cell proliferation, and tissue remodeling. Melatonin (MLT) and its - and -substituted derivatives are known to exhibit potent antioxidant and anti-inflammatory properties; however, their specific therapeutic mechanisms in wound healing remain largely unexplored. Therefore, this study aimed to investigate the potential wound-healing properties of MLT and its six derivatives using an integrated computational and in vitro validation approach. Potential targets of MLT and its derivatives were screened using SwissTargetPrediction (version 2023 release) and SuperPred (version 3.0), yielding 491 candidate targets. These targets were cross-referenced with the GeneCards (version 5.24.0) database to map their involvement across the four phases of wound healing: hemostasis, inflammation, proliferation, and remodeling. Network interaction models were constructed using Cytoscape (version 3.10.3) and GeneMANIA (version 3.6.0), and pathway enrichment was analyzed using the ShinyGO (version 0.85.1) platform. Enrichment analysis prioritized HIF-1-related signaling as a candidate regulatory axis associated with the predicted targets of melatonin derivatives across the inflammatory, proliferative, and remodeling phases of wound healing. In vitro validation using normal human dermal fibroblasts (NHDFs) demonstrated that all compounds, at non-toxic concentrations, significantly enhanced cell viability, as measured by the MTT assay. Furthermore, wound scratch assays revealed that the -bromobenzoyl-substituted derivative (EBMLT) accelerated cell migration, achieving complete wound gap closure within 24 h and outperforming the parent compound. Molecular docking simulations using AutoDock 4.2 predicted favorable binding interactions of the derivatives toward key wound healing-related targets (NF-κB, EGFR, VEGFR-1, MMP-1, and MMP-13). Aromatic-substituted derivatives (BMLT, BBMLT, and EBMLT) exhibited more favorable predicted binding interactions than the parent compound across all targets, whereas the aliphatic-substituted derivative (SMLT) showed weaker predicted interactions, particularly with VEGFR-1. These findings suggest that - and -aromatic substitutions are associated with more favorable binding interactions. Notably, the -bromobenzoyl derivative (EBMLT) exhibited the most potent wound-closure activity, highlighting it as a candidate compound for wound-healing applications. - Source: PubMed
Publication date: 2026/07/27
Siriparu PimolwanSungthong BunleuPuthongking Ploenthip - Precise mitochondrial targeting in chondrocytes is essential for interrupting the vicious cycle of oxidative stress and cartilage degeneration in osteoarthritis (OA). Here, we develop a biomimetic nanoplatform (CM@SS31-Se) with dual targeting capability. This system comprises selenium nanoparticles with glutathione peroxidase mimetic activity as the antioxidant core, SS31 peptide for mitochondrial homing, and chondrocyte membrane coating for homotypic recognition. Following intra-articular injection, the nanoplatform demonstrates prolonged joint retention up to 14 days with favorable biocompatibility. Functionally, the outer membrane shell facilitates chondrocyte internalization through homotypic recognition, the SS31 peptide promotes mitochondrial accumulation through its cardiolipin binding affinity, and the selenium core subsequently provides sustained mtROS scavenging. These dual-targeting properties restore mitochondrial membrane potential and ATP synthesis, upregulate anabolic markers (SOX9, Col II, Aggrecan), and downregulate MMP13 and pro-inflammatory mediators, ultimately promoting the restoration of a regenerative phenotype in degenerative chondrocytes. Thus, this biomimetic nanoplatform enables guided mitochondrial functional restoration, demonstrating therapeutic potential for attenuating OA progression. - Source: PubMed
Publication date: 2026/08/12
Zhang ZihanDu QianZhu ZiyinZhu ZhitongHe JialinXin ZhijunDeng Jiang - The avascular and alymphatic nature of articular cartilage severely limits its intrinsic repair capacity. Even when spontaneous healing occurs, it inevitably culminates in fibrocartilage formation, which lacks the biomechanical functionality of native hyaline cartilage. Mesenchymal stem cells (MSCs) have emerged as a promising therapeutic candidate owing to their regenerative potential. However, direct intra-articular transplantation exposes MSCs to a hostile microenvironment characterized by excessive reactive oxygen species and pro-inflammatory cytokines, leading to extensive apoptosis and substantially compromised therapeutic efficacy. Cell-derived decellularized extracellular matrix (dE) has been shown to enhance chondrogenic potential, yet it fails to suppress hypertrophic differentiation during chondrogenic induction, a major hurdle in cartilage engineering. To overcome this bottleneck, we integrated ascorbic acid (AA) with dE preconditioning. Notably, concurrent dE and AA combination synergistically enhanced antioxidant capacity during expansion, while significantly attenuating hypertrophic markers and matrix catabolism (MMP13, IL-1β) during chondrogenic induction. Mechanistically, this strategy sustained TGF-β receptor I expression alongside endogenous TGF-β1 ligand downregulation, optimizing canonical signaling without pathological overactivation. Strikingly, antecedent AA priming reversed these benefits, compromising chondrogenic potential and exacerbating hypertrophy during chondrogenic induction, underscoring a stringent temporal dependency. Collectively, this biomaterial-guided preconditioning strategy generates chondroprogenitors with reduced hypertrophic markers and improved hyaline phenotype in vitro, warranting further preclinical in vivo investigation. - Source: PubMed
Publication date: 2026/08/06
Wei ZhixinYu QingqingLiao DongfaSong BenjingGou XueXie QingyunGuo TailinChen Song