Mechanical forces in skin disorders. Issue 3 (June 2018)
- Record Type:
- Journal Article
- Title:
- Mechanical forces in skin disorders. Issue 3 (June 2018)
- Main Title:
- Mechanical forces in skin disorders
- Authors:
- Hsu, Chao-Kai
Lin, Hsi-Hui
Harn, Hans I-Chen
Hughes, Michael W.
Tang, Ming-Jer
Yang, Chao-Chun - Abstract:
- Abstract: Mechanical forces are known to regulate homeostasis of the skin and play a role in the pathogenesis of skin diseases. The epidermis consists of keratinocytes that are tightly adhered to each other by cell junctions. Defects in keratins or desmosomal/hemidesmosomal proteins lead to the attenuation of mechanical strength and formation of intraepidermal blisters in the case of epidermolysis bullosa simplex. The dermis is rich in extracellular matrix, especially collagen, and provides the majority of tensile force in the skin. Keloid and hypertrophic scar, which is the result of over-production of collagen by fibroblasts during the wound healing, are associated with extrinsic tensile forces and changes of intrinsic mechanical properties of the cell. Increasing evidences shows that stiffness of the skin environment determines the regenerative ability during wound healing process. Mechanotransduction pathways are also involved in the morphogenesis and cyclic growth of hair follicles. The development of androgenetic alopecia is correlated to tensile forces generated by the fibrous tissue underlying the scalp. Acral melanoma predominantly occurs in the weight-bearing area of the foot suggesting the role of mechanical stress. Increased dermal stiffness from fibrosis might be the cause of recessive dystrophic epidermolysis bullosa associated squamous cell carcinoma. Strategies to change the mechanical forces or modify the mechanotransduction signals may lead to a new way toAbstract: Mechanical forces are known to regulate homeostasis of the skin and play a role in the pathogenesis of skin diseases. The epidermis consists of keratinocytes that are tightly adhered to each other by cell junctions. Defects in keratins or desmosomal/hemidesmosomal proteins lead to the attenuation of mechanical strength and formation of intraepidermal blisters in the case of epidermolysis bullosa simplex. The dermis is rich in extracellular matrix, especially collagen, and provides the majority of tensile force in the skin. Keloid and hypertrophic scar, which is the result of over-production of collagen by fibroblasts during the wound healing, are associated with extrinsic tensile forces and changes of intrinsic mechanical properties of the cell. Increasing evidences shows that stiffness of the skin environment determines the regenerative ability during wound healing process. Mechanotransduction pathways are also involved in the morphogenesis and cyclic growth of hair follicles. The development of androgenetic alopecia is correlated to tensile forces generated by the fibrous tissue underlying the scalp. Acral melanoma predominantly occurs in the weight-bearing area of the foot suggesting the role of mechanical stress. Increased dermal stiffness from fibrosis might be the cause of recessive dystrophic epidermolysis bullosa associated squamous cell carcinoma. Strategies to change the mechanical forces or modify the mechanotransduction signals may lead to a new way to treat skin diseases and promote skin regeneration. … (more)
- Is Part Of:
- Journal of dermatological science. Volume 90:Issue 3(2018)
- Journal:
- Journal of dermatological science
- Issue:
- Volume 90:Issue 3(2018)
- Issue Display:
- Volume 90, Issue 3 (2018)
- Year:
- 2018
- Volume:
- 90
- Issue:
- 3
- Issue Sort Value:
- 2018-0090-0003-0000
- Page Start:
- 232
- Page End:
- 240
- Publication Date:
- 2018-06
- Subjects:
- Mechanical forces -- Mechanobiology -- Epidermolysis bullosa simplex -- Keloid -- Alopecia -- Regeneration
Dermatology -- Periodicals
Skin Diseases -- Periodicals
Dermatologie -- Périodiques
616.5005 - Journal URLs:
- http://www.elsevier.com/journals ↗
http://www.sciencedirect.com/science/journal/09231811 ↗ - DOI:
- 10.1016/j.jdermsci.2018.03.004 ↗
- Languages:
- English
- ISSNs:
- 0923-1811
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 4968.766500
British Library DSC - BLDSS-3PM
British Library HMNTS - ELD Digital store - Ingest File:
- 9184.xml