loading...| Preferred Name |
Skin Aging |
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| Synonyms |
PathwayType: signaling PMID: 25906193 Description: Photoaging refers to the cumulative specific alterations in the skin caused by chronic exposure to sunlight. Pathway is built manually using published studies. PMID: 26215577 NodeType: Pathway Link: https://mammal-profservices.pathwaystudio.com/app/sd?urn=urn:agi-pathway:uuid-9598959d-27c8-42bb-a9bc-e89fe662921d Pathway_Author: V. Sobolev ORCID:0000-0003-4779-156X Organ_System: integumentary system CellType: fibroblast PMID: 16849327 Notes: Headnote: Photoaging refers to the cumulative specific alterations in the skin caused by chronic exposure to sunlight. The process involves prominent cutaneous transformation that is clinically characterized by fine and coarse wrinkles, blotchy dyspigmentation, telangiectasia, sallowness, increased fragility, and rough skin texture and depends on both environmental and intrinsic factors, with fair-skinned individuals showing more pronounced symptoms of photoaging than people with darker skin. Photoaging results from long-term continuous exposure of the skin to ultraviolet (UV) radiation of approximately 300-400 nm. Signaling description: Upon exposure to UV radiation, reactive oxygen species (ROS) are formed in the skin. These ROS can activate the epidermal growth factor receptor (EGFR) and cytokine receptors on the surface of fibroblasts and keratinocytes. Further, the activated receptors stimulate p38 and JNK, members of the MAPK signaling cascade. As a result, c-Fos and c-Jun form AP-1 which stimulates the matrix metalloproteinase (MMP) transcription. Increased MMP transcription accelerates collagen degradation leading to dermal matrix alterations. The EGFR activation has been shown to be crucial for a wide range of UV irradiation-induced responses. EGFR is maintained in an inactive state by protein tyrosine phosphatase kappa (PTPRK), which is inhibited by UV rays, thereby allowing EGFR to become activated. Tumor necrosis factor-alpha (TNF-a) is a proinflammatory cytokine produced in the skin in response to ultraviolet B radiation (UVB) in both keratinocytes and dermal fibroblasts. In case of an extensive exposure to sunlight, increased amounts of TNF-a are produced leading to a systemic effect which, includes UVB-induced apoptosis and the removal of damaged cells. Outcome effects: UV exposure may lead to the induction of receptors for epidermal growth factor, cytokines, and TNF-a in in the skin cells, which eventually causes collagen degradation via the induction of the MAPK signaling cascade, as well as DNA degradation and the UV-induced apoptosis. Highlighted proteins: Proteins with decreased expression or activity are highlighted in blue. Proteins with increased expression or activity are highlighted in red. MMP1, MMP2, MMP3, MMP9, MAP3K1 and ROS are highlighted in red in order to emphasize the increase of the ECM degradation and DNA Damage. Source: Diseases |
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| ID |
urn:agi-pathway:uuid-9598959d-27c8-42bb-a9bc-e89fe662921d |
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| database_cross_reference |
PS:PathwayType PS:Description PS:Pathway_Author PS:Link PS:CellType PS:Organ_System PS:PMID PS:NodeType PS:Notes PS:Source |
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| has_exact_synonym |
PathwayType: signaling PMID: 25906193 Description: Photoaging refers to the cumulative specific alterations in the skin caused by chronic exposure to sunlight. Pathway is built manually using published studies. PMID: 26215577 NodeType: Pathway Pathway_Author: V. Sobolev ORCID:0000-0003-4779-156X Organ_System: integumentary system CellType: fibroblast PMID: 16849327 Notes: Headnote: Photoaging refers to the cumulative specific alterations in the skin caused by chronic exposure to sunlight. The process involves prominent cutaneous transformation that is clinically characterized by fine and coarse wrinkles, blotchy dyspigmentation, telangiectasia, sallowness, increased fragility, and rough skin texture and depends on both environmental and intrinsic factors, with fair-skinned individuals showing more pronounced symptoms of photoaging than people with darker skin. Photoaging results from long-term continuous exposure of the skin to ultraviolet (UV) radiation of approximately 300-400 nm. Signaling description: Upon exposure to UV radiation, reactive oxygen species (ROS) are formed in the skin. These ROS can activate the epidermal growth factor receptor (EGFR) and cytokine receptors on the surface of fibroblasts and keratinocytes. Further, the activated receptors stimulate p38 and JNK, members of the MAPK signaling cascade. As a result, c-Fos and c-Jun form AP-1 which stimulates the matrix metalloproteinase (MMP) transcription. Increased MMP transcription accelerates collagen degradation leading to dermal matrix alterations. The EGFR activation has been shown to be crucial for a wide range of UV irradiation-induced responses. EGFR is maintained in an inactive state by protein tyrosine phosphatase kappa (PTPRK), which is inhibited by UV rays, thereby allowing EGFR to become activated. Tumor necrosis factor-alpha (TNF-a) is a proinflammatory cytokine produced in the skin in response to ultraviolet B radiation (UVB) in both keratinocytes and dermal fibroblasts. In case of an extensive exposure to sunlight, increased amounts of TNF-a are produced leading to a systemic effect which, includes UVB-induced apoptosis and the removal of damaged cells. Outcome effects: UV exposure may lead to the induction of receptors for epidermal growth factor, cytokines, and TNF-a in in the skin cells, which eventually causes collagen degradation via the induction of the MAPK signaling cascade, as well as DNA degradation and the UV-induced apoptosis. Highlighted proteins: Proteins with decreased expression or activity are highlighted in blue. Proteins with increased expression or activity are highlighted in red. MMP1, MMP2, MMP3, MMP9, MAP3K1 and ROS are highlighted in red in order to emphasize the increase of the ECM degradation and DNA Damage. Source: Diseases |
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| id |
urn:agi-pathway:uuid-9598959d-27c8-42bb-a9bc-e89fe662921d |
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| label |
Skin Aging |
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| notation |
uuid-9598959d-27c8-42bb-a9bc-e89fe662921d |
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| prefLabel |
Skin Aging |
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| treeView |
urn:agi-folder:aging_related_diseases urn:agi-folder:s urn:agi-folder:skin_aging urn:agi-folder:integumentary_system |
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| subClassOf |
urn:agi-folder:aging_related_diseases urn:agi-folder:s urn:agi-folder:skin_aging urn:agi-folder:integumentary_system |