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
- Intervertebral disc degeneration (IVDD) is a major cause of chronic low back pain, thus therapies capable of halting its progression are urgently needed. Evidence suggests that oxidative stress is a key accelerator of IVDD, making interventions targeting reactive oxygen species (ROS) highly promising. The natural compound 6-gingerol has been proved to possess potent antioxidant properties, however, its therapeutic application is hampered by poor solubility, rapid clearance, and lack of targeted delivery. To address these limitations and investigate the effect of 6-gingerol on IVDD, we developed an integrated nanoplatform (H@G) by encapsulating 6-gingerol within hollow manganese dioxide nanoparticles. The synthesized H@G nanoparticles exhibited a uniform hollow spherical structure (∼100 nm), a high surface area, and successful drug loading without altering the carrier morphology. The nanoparticles demonstrated good stability in physiological media but underwent rapid degradation under acidic conditions and in an HO microenvironment. Accordingly, H@G exhibited pH- and HO-responsive drug release. The H@G nanoparticles also displayed superoxide dismutase-like, hydroxyl radical-scavenging, and catalase-like activities in a concentration-dependent manner. Under HO-induced oxidative stress, H@G significantly enhanced the viability of nucleus pulposus cells, potently scavenged both intracellular and mitochondrial ROS, restored mitochondrial membrane potential, and preserved cristae ultrastructure. Furthermore, H@G restored extracellular matrix homeostasis under oxidative stress by upregulating anabolic markers (ACAN and COL2A1) and downregulating catabolic enzymes (MMP3 and MMP13). Collectively, our results demonstrate that the H@G nanosystem effectively attenuates oxidative stress, maintains mitochondrial homeostasis, and promotes matrix anabolism in NPCs, which provides a promising and targeted strategy to attenuate oxidative stress and disc degeneration in IVDD. - Source: PubMed
Publication date: 2026/05/22
Liu XuLu BolinZhou YunqiZhang ChengdongShi FengFeng GangLuo XuweiXiao Dongqin - Osteoarthritis (OA), a degenerative joint disease driven by synovial inflammation, oxidative stress and progressive cartilage degradation, remains a major clinical challenge. While drug-loaded nanozymes offer an effective strategy for OA treatment by scavenging reactive oxygen species (ROS) and delivering therapeutics, their efficacy is limited by insufficient catalytic activity and poor drug retention capacity. Herein, we developed a specific matrix metalloproteinase (MMP) 13-responsive smart nanogel system (M-MA@KSPB) comprising a selenium-doped Prussian blue nanozyme (SPB) core loaded with kartogenin (KGN) and an MMP13-responsive peptide cross-linking hyaluronic acid methacryloyl (HAMA) shell. As MMP13 is a key biomarker of OA progression, the MMP13-triggered responsiveness of M-MA@KSPB enhanced its retention within the joint cavity through targeted structural changes, thereby enabling spatiotemporally precise KGN release for cartilage regeneration. Upon release, the SPB nanozyme exhibited catalase (CAT)-, superoxide dismutase (SOD)-, and glutathione reductase (GR)-like activities, potently scavenging ROS and mitigating oxidative stress. Furthermore, the M-MA@KSPB downregulated pro-inflammatory cytokines (TNF-α, IL-6), while enhancing collagen II synthesis and suppressing MMP13 expression in Lipopolysaccharide (LPS)-stimulated chondrocytes. In a post-traumatic OA rat model, this system inhibited joint inflammation and osteophyte formation, concurrently promoting cartilage regeneration and restoring anabolic/catabolic balance through KGN-mediated repair. This nanogel system offers a new OA treatment strategy by combining anti-oxidative stress therapy with cartilage repair. - Source: PubMed
Publication date: 2026/05/26
Song YuanxiZhu XiuzhenYu NaBian XiaoliYang DongyiMa LanLanZhang MinYang JianhongZuo Wenbao - To investigate the effect of synovial mesenchymal stem cell (SMSC) derived extracellular vesicles (EVs) long non-coding ribonucleic acid (LncRNA) nuclear small RNA host gene 14 (SNHG14) on chondrocyte injury and its potential mechanism. - Source: PubMed
Publication date: 2026/05/15
Zou ShaoBo - To explore the mechanism mediating the ameliorative effect of Granules on cartilage injury in knee osteoarthritis (KOA). - Source: PubMed
Cheng YuanyuanHuang ChuanbingZhang JuanZhu YawenQian Ai - : Allomyrinasin is a cationic antimicrobial peptide derived from larvae with known antibacterial and anti-inflammatory properties; however, its effects on migration-related mechanisms in oral squamous cell carcinoma (OSCC) remain poorly understood. This study investigated the anti-migratory potential of allomyrinasin in OSCC cells, focusing on Na/HCO cotransporter (NBC) activity as a key migratory module. : NBC activity was assessed in YD-38 OSCC cells treated with allomyrinasin. Cell migration was evaluated by wound healing and Transwell assays, and MMP expression. Intracellular reactive oxygen species (ROS), apoptosis-related markers, and lamin A/C expression were analyzed using fluorescence-based assays and gene expression analysis. : Allomyrinasin inhibited NBC activity and suppressed cell migration without substantial loss of cell viability. was selectively downregulated among the tested MMPs. Lamin A/C expression was markedly upregulated, suggesting enhanced nuclear stiffness that may restrict confined cell migration. Intracellular ROS levels were elevated, and apoptotic progression was confirmed by increased Annexin V/PI positivity along with downregulation of B-cell lymphoma 2 () and upregulation of BCL-2-associated X genes (), through a p53-independent pathway consistent with the -deleted status of YD-38 cells. : Allomyrinasin suppresses OSCC cell migration by targeting NBC activity as a key component of the migratory machinery, accompanied by oxidative stress induction and pro-apoptotic signaling. These findings identify allomyrinasin as a potential anti-migratory therapeutic candidate and highlight NBC activity as a promising target for attenuating cancer metastasis. - Source: PubMed
Publication date: 2026/05/19
Prismasari SeptikaKim Hyeong JaeHong Jeong HeeKang Jung Yun