Metaloproteinasas y piel

Increased fibroblast proliferation and activity after applying intense pulsed light 800–1200nm

“…Metalloproteinases (MMP) are endopeptidases that perform a degradative function, generally targeting the extracellular matrix (Perez-Garcia, 2004). MMP1 is called collagenase and its main substrate are collagen type III, I, II, VII and X (Li et al, 2014).…”

Cosmetic Topical Use of Vitamin C

“…MMPs are proteolytic enzymes that are responsible for remodeling the extracellular matrix and that together can degrade all its constituents [21]. UV radiation triggers the production of pro-inflammatory cytokines that favor the expression of MMP-1, MMP-3, MMP-9, and MMP-12, which, as we have seen, accelerate the degradation of collagen, and favor the accumulation of elastin, generating manifestations of some signs of photoaging such as hyperpigmentation, telangiectasias, coarse skin texture, deep wrinkles, and solar elastosis [20,22]. As MMPs also promote angiogenesis as a result of this stimulation, they favor cancer cell growth and spread (Figure 5) [23].…”

“…• It inhibits the action of protein transcription factor-1 (aP1) (see paragraph 8), acting vitamin C as a regulator of the MMP, and, therefore, decreasing the damage that these MMPs produce to collagen fibers [18][19][20][21][22][23].…”

Use of Intralesional and Perilesional Human Recombinant Epidermal Growth Factor (hrEGF) in the Local Treatment of Venous Ulcer – Review Article – Expert Recommendation

“…Its activity is hampered by protease inhibitors, including tissue inhibitors of metalloproteinases (TIMP) and α-2-macroglobulin, 17 and its regulation is carried out by different actors including among others the epidermal growth factor, which have immunohistochemistry degradation, and their imbalance causes an uncontrolled proteolysis characteristic of a chronic inflammatory state. [17][18][19] Furthermore, in chronic ulcers, fibroblast dysfunctions such as increased apoptosis, premature senescence, senescence-like phenotype, or poor growth response in the absence of senescence markers have been reported. Some of these differential dysfunctions may be secondary to differences in the age or sex of the patient, the size, or the duration of the ulcer.…”