title: Endothelial dysfunction and mechanobiology in pathological cutaneous scarring: lessons learned from soft tissue fibrosis.
abstract: Hypertrophic scars/keloids are pathogenic scars that are characterized by collagen and fibroblast accumulation. The endothelia in the lesions are mechanosensitive and participate actively in the pathogenesis of these scars. The present review summarizes how endothelium responds to mechanical stimuli such as shear, stretch and hydrostatic pressure. It also shows that in heart, liver, kidney and lung fibrosis, endothelial dysfunctions (EDs) associate with changes in vascular tone, endothelial permeability, coagulation and vasomodulation that result in inflammation, hypertension and coagulation. Pathological scars exhibit similar EDs during their development and progression. Mechanopharmaceutical or mechanotherapeutic interventions that rescue EDs may be useful scar treatments.
authors.affiliation: Department of Dermatology, Beijing Tsinghua Changgung Hospital, Tsinghua University, Beijing, 102218, China.|Department of Plastic Surgery, Meitan General Hospital, Beijing, 100028, China.
authors.forename: C
authors.identifier: http://orcid.org/0000-0001-9521-5650
authors.initials: C
authors.lastname: Huang
authors.affiliation: Department of Biomedical Engineering, School of Medicine, Tsinghua University, Beijing, 100084, China.
authors.forename: L
authors.initials: L
authors.lastname: Liu
authors.affiliation: Department of Biomedical Engineering, School of Medicine, Tsinghua University, Beijing, 100084, China.
authors.forename: Z
authors.initials: Z
authors.lastname: You
authors.affiliation: Department of Dermatology, Beijing Tsinghua Changgung Hospital, Tsinghua University, Beijing, 102218, China.
authors.forename: Y
authors.initials: Y
authors.lastname: Zhao
authors.affiliation: Department of Hepatobiliary Surgery, Beijing Tsinghua Changgung Hospital, Tsinghua University, Beijing, 102218, China.
authors.forename: J
authors.initials: J
authors.lastname: Dong
authors.affiliation: Department of Biomedical Engineering, School of Medicine, Tsinghua University, Beijing, 100084, China.
authors.forename: Y
authors.initials: Y
authors.lastname: Du
authors.affiliation: Department of Plastic, Reconstructive and Aesthetic Surgery, Nippon Medical School, Tokyo, 113-8603, Japan.
authors.forename: R
authors.initials: R
authors.lastname: Ogawa
mesh_terms: D000818:Animals; D050197:Atherosclerosis / Q000473:pathology / Q000503:physiopathology; D001696:Biomechanical Phenomena / Q000502:physiology; D017439:Cicatrix, Hypertrophic / Q000473:pathology* / Q000503:physiopathology; D003238:Connective Tissue / Q000473:pathology*; D004195:Disease Models, Animal; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005355:Fibrosis / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D007668:Kidney / Q000473:pathology; D008103:Liver Cirrhosis / Q000473:pathology / Q000503:physiopathology; D008168:Lung / Q000473:pathology; D051379:Mice; D012595:Scleroderma, Systemic / Q000473:pathology / Q000503:physiopathology; D013552:Swine