title: Soft tissue mechanotransduction in wound healing and fibrosis.
abstract: Recent evidence suggests that mechanical forces can significantly impact the biologic response to injury. Integrated mechanical and chemical signaling networks have been discovered that enable physical cues to regulate disease processes such as pathologic scar formation. Distinct molecular mechanisms control how tensional forces influence wound healing and fibrosis. Conceptual frameworks to understand cutaneous repair have expanded beyond traditional cell-cytokine models to include dynamic interactions driven by mechanical force and the extracellular matrix. Strategies to manipulate these biomechanical signaling networks have tremendous therapeutic potential to reduce scar formation and promote skin regeneration.
authors.affiliation: Hagey Laboratory for Pediatric Regenerative Medicine, Division of Plastic and Reconstructive Surgery, Department of Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA.
authors.forename: Victor W
authors.initials: VW
authors.lastname: Wong
authors.forename: Michael T
authors.initials: MT
authors.lastname: Longaker
authors.forename: Geoffrey C
authors.initials: GC
authors.lastname: Gurtner
mesh_terms: D001696:Biomechanical Phenomena; D002450:Cell Communication; D002921:Cicatrix / Q000517:prevention & control; D005109:Extracellular Matrix / Q000378:metabolism; D005347:Fibroblasts / Q000378:metabolism / Q000473:pathology; D006801:Humans; D040542:Mechanotransduction, Cellular; D062326:Re-Epithelialization / Q000502:physiology; D012038:Regeneration / Q000502:physiology*; D012867:Skin / Q000293:injuries / Q000378:metabolism* / Q000473:pathology; D017695:Soft Tissue Injuries / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology*; D014945:Wound Healing / Q000502:physiology*