MMPs are  secreted by invasive (migrating) cancer cells, researchers are investigating synthetic therapeutic agents that inhibit the activity of MMPs to control the spread of cancer cells.
 Phagocytotic degradation occurs intracellularly and involves macrophages to remove components of the ECM. Fibroblasts are also capable of phagocytosing and degrading collagen fibrils within the lysosomes of the cell.
FOLDER 6.1 Clinical Correlation: Collagenopathies
The important role of collagens in the body can be illus-trated by collagenopathies (collagen diseases), which are caused by a deficit or abnormality in the production of collagens. In the future, gene therapy could potentially be used either to control deposition of faulty collagen or to reverse the disease process caused by the mutated genes.
specific collagens. Most collagenopathies are attributed to The following table lists the most common collagenopathies mutations in genes encoding the chains in the various that occur in humans.
The Most Common Collagenopathies in Humans Type of Collagen Disease Symptoms I Osteogenesis imperfecta Repeated fractures after minor trauma, brittle bones, abnormal teeth, thin skin, weak tendons, blue sclerae, progressive hearing loss II Kniest dysplasia; Short stature, restricted joint mobility, ocular changes Achondrogenesis, type 2 leading to blindness, wide metaphyses, and  joint abnormality seen in radiographs III Ehlers-Danlos type IV Hypermobility of joints of digits, pale thin skin, severe bruisability, early morbidity and mortality, resulting from rupture of vessels and internal organs IV Alport’s syndrome Hematuria resulting from structural changes in the glomerular basement membrane of the kidney, progressive hearing loss, and ocular lesions VII Kindler’s syndrome Severe blistering and scarring of the skin after minor trauma, resulting from absence of anchoring fibrils IX Multiple ephiphyseal dysplasia Skeletal deformations resulting from impaired (MED) endochondral ossification and dysplasia (MED), premature degenerative joint disease X Schmid metaphysal Skeletal deformations characterized by modifications chondrodysplasia of the vertebral bodies and chondrodysplasia metaphyses of the long bone XI Weissenbacher-Zweymuller Similar clinical features to type II collagenopathies syndrome Stickler’s syndrome  in addition to craniofacial and skeletal deformations, (includes also additional mutations   severe myopia, retinal detachment, and progressive of type II collagen gene) hearing loss XVII Generalized atrophic benign Blistering skin disease with mechanically induced epidermolysis bullosa (GABEB) dermal–epidermal separation, epidermolysis bullosa resulting from faulty hemidesmosomes, skin atrophy, nail dystrophy, and alopecia
Reticular fibers provide a supporting framework for the cellular constituents of various tissues and organs.
Reticular fbers and collagen type I fibers share a prominent feature. They both consist of collagen fibrils. Unlike collagen fibers, however, reticular fibers are composed of type III collagen. The individual fibrils that constitute a reticular fiber exhibit a 68-nm banding pattern (the same as the fibrils of type I collagen). The fibrils have a narrow diameter (about 20 nm), exhibit a branching pattern, and typically do not bundle to form thick fibers.