Peer-reviewed papers from 1994 to 2025 on MMP13 and the ingredients studied against it. Each is labelled with the kind of evidence it is, and links straight to PubMed.
Elevated glucose promotes MMP13 and ADAMTS5 production by osteoarthritic chondrocytes under oxygenated but not hypoxic conditions.
Differential Effects of Hypoxia versus Hyperoxia or Physoxia on Phenotype and Energy Metabolism in Human Chondrocytes from Osteoarthritic Compared to Macroscopically Normal Cartilage.
Concentration-dependent effects of leptin on osteoarthritis-associated changes in phenotype of human chondrocytes.
Overview of MMP-13 as a Promising Target for the Treatment of Osteoarthritis.
ADAMTS5 in Osteoarthritis: Biological Functions, Regulatory Network, and Potential Targeting Therapies.
Altered expression of the core circadian clock component PERIOD2 contributes to osteoarthritis-like changes in chondrocyte activity.
Basic Calcium Phosphate Crystals Induce Osteoarthritis-Associated Changes in Phenotype Markers in Primary Human Chondrocytes by a Calcium/Calmodulin Kinase 2-Dependent Mechanism.
The chondrocyte-intrinsic circadian clock is disrupted in human osteoarthritis.
Radiocarbon dating reveals minimal collagen turnover in both healthy and osteoarthritic human cartilage.
New hope for the treatment of osteoarthritis through selective inhibition of MMP-13.
The tissue inhibitors of metalloproteinases (TIMPs): an ancient family with structural and functional diversity.
Matrix metalloproteinase 13-deficient mice are resistant to osteoarthritic cartilage erosion but not chondrocyte hypertrophy or osteophyte development.
Development of musculoskeletal toxicity without clear benefit after administration of PG-116800, a matrix metalloproteinase inhibitor, to patients with knee osteoarthritis: a randomized, 12-month, double-blind, placebo-controlled study.
Increased matrix metalloproteinase-13 production with aging by human articular chondrocytes in response to catabolic stimuli.
Deletion of active ADAMTS5 prevents cartilage degradation in a murine model of osteoarthritis.
Matrix homeostasis in aging normal human ankle cartilage.
Collagen of articular cartilage.
Postnatal expression in hyaline cartilage of constitutively active human collagenase-3 (MMP-13) induces osteoarthritis in mice.
Effect of collagen turnover on the accumulation of advanced glycation end products.
Interleukin-1 induction of collagenase 3 (matrix metalloproteinase 13) gene expression in chondrocytes requires p38, c-Jun N-terminal kinase, and nuclear factor kappaB: differential regulation of collagenase 1 and collagenase 3.
Cloning, expression, and type II collagenolytic activity of matrix metalloproteinase-13 from human osteoarthritic cartilage.
The new collagenase, collagenase-3, is expressed and synthesized by human chondrocytes but not by synoviocytes. A role in osteoarthritis.
Biochemical characterization of human collagenase-3.
Degradation of cartilage aggrecan by collagenase-3 (MMP-13).
Molecular cloning and expression of collagenase-3, a novel human matrix metalloproteinase produced by breast carcinomas.
A Standardized Boswellia serrata Extract Improves Knee Joint Function and Cartilage Morphology in Human Volunteers with Mild to Moderate Osteoarthritis in a Randomized Placebo-Controlled Study.
Efficacy and Safety of Boswellia serrata and Apium graveolens L. Extract Against Knee Osteoarthritis and Cartilage Degeneration: A Randomized, Double-blind, Multicenter, Placebo-Controlled Clinical Trial.
Acetyl-11-keto-beta-boswellic acid ameliorates monosodium iodoacetate-induced osteoarthritis in rats: implications of HMGB1/TLR4/NF-κB and Nrf2/HO-1.
Boswellia serrata Extract, 5-Loxin®, Prevents Joint Pain and Cartilage Degeneration in a Rat Model of Osteoarthritis through Inhibition of Inflammatory Responses and Restoration of Matrix Homeostasis.
Boswellia frereana (frankincense) suppresses cytokine-induced matrix metalloproteinase expression and production of pro-inflammatory molecules in articular cartilage.
Comparative efficacy and tolerability of 5-Loxin and Aflapin Against osteoarthritis of the knee: a double blind, randomized, placebo controlled clinical study.
A double blind, randomized, placebo controlled study of the efficacy and safety of 5-Loxin for treatment of osteoarthritis of the knee.
Curcumin and omega-3 ameliorate experimental osteoarthritis progression in terms of joint pain and mitochondrial dysfunction.
Curcumin monoglucuronide protects cartilage from progressive degeneration by blocking MMP-13.
Regulation of type II collagen, matrix metalloproteinase-13 and cell proliferation by interleukin-1β is mediated by curcumin via inhibition of NF-κB signaling in rat chondrocytes.
Influence of piperine on the pharmacokinetics of curcumin in animals and human volunteers.
The epigenetic effect of glucosamine and a nuclear factor-kappa B (NF-kB) inhibitor on primary human chondrocytes--implications for osteoarthritis.
Glucosamine promotes chondrogenic phenotype in both chondrocytes and mesenchymal stem cells and inhibits MMP-13 expression and matrix degradation.
Glucosamine sulfate modulates the levels of aggrecan and matrix metalloproteinase-3 synthesized by cultured human osteoarthritis articular chondrocytes.
Chondroitin Sulfate Enhances Proliferation and Migration via Inducing β-Catenin and Intracellular ROS as Well as Suppressing Metalloproteinases through Akt/NF-κB Pathway Inhibition in Human Chondrocytes.
Hyaluronan inhibits matrix metalloproteinase-13 in human arthritic chondrocytes via CD44 and P38.
Vitamin C Protects Chondrocytes against Monosodium Iodoacetate-Induced Osteoarthritis by Multiple Pathways.
Oral administration of N-acetyl cysteine prevents osteoarthritis development and progression in a rat model.
No studies match that search.
People, usually against a placebo. The strongest evidence here, but it tests one extract at one dose.
Cartilage cells or tissue from human donors, often from joint replacements, studied in a dish.
Usually rats with induced joint damage. Useful for mechanism; doses and biology differ from ours.
Cell lines or tissue samples. Shows how a compound can act, not what it does in a body.