977 The wound healing of fractional photothermolysis mimicks scarless healing with minimal myofibroblast activation

In recent years, research on wound healing has become increasingly in-depth, but therapeutic effects are still not satisfactory. Occasionally, pathological tissue repair occurs. Influencing factors have been proposed, but finding the turning point between normal and pathological tissue repair is difficult. Therefore, we focused our attention on the most basic level of tissue repair: fibroblasts. Fibroblasts were once considered terminally differentiated cells that represent a single cell type, and their heterogeneity was not studied until recently. We believe that subpopulations of fibroblasts play different roles in tissue repair, resulting in different repair results, such as the formation of normal scars in physiological tissue repair and fibrosis or ulcers in pathological tissue repair. It is also proposed that scarless healing can be achieved by regulating fibroblast subpopulations.

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Immunohistochemical investigation of wound healing in response to fractional photothermolysis

Journal of Biomedical Optics ◽

10.1117/1.3275479 ◽

2009 ◽

Vol 14 (6) ◽

pp. 064044 ◽

Cited By ~ 32

Author(s):

Doris Helbig ◽

Marc Oliver Bodendorf ◽

Sonja Grunewald ◽

Michael Kendler ◽

Jan C. Simon ◽

...

Keyword(s):

Wound Healing ◽

Immunohistochemical Investigation ◽

Fractional Photothermolysis

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Fetal Wound Healing

Textbook on Scar Management ◽

10.1007/978-3-030-44766-3_1 ◽

2020 ◽

pp. 3-9

Author(s):

Magda M. W. Ulrich

Keyword(s):

Wound Healing ◽

Animal Studies ◽

Healing Process ◽

Intrinsic Property ◽

Wound Healing Process ◽

Skin Wounds ◽

Fetal Skin ◽

Uterine Environment ◽

Fetal Wound ◽

Scarless Healing

AbstractFirst- and second-trimester fetal skin wounds are known to heal without scarring.Research has excluded factors like the sterile uterine environment as the cause of scarless repair, and it is believed that scarless healing is an intrinsic property of early fetal skin. However, increasing wound size and induction of the inflammatory reaction can evoke a scar response in the fetus.For decades, research is performed to elucidate the mechanisms responsible for scarless healing in fetuses. Much research has been performed in animal studies, and several mechanisms have been proposed to be involved such as the microenvironment and the extracellular matrix, a reduced inflammatory response, differences in growth factor profile, and differences in fibroblast phenotype.It is clear that the wound healing process leading to scarless healing cannot be attributed to just one factor or mechanism but will be the result of a complex of interconnected processes.This chapter describes some of the possible mechanisms which may play a role in scarless healing.

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A Review of Fetal Scarless Healing

ISRN Dermatology ◽

10.5402/2012/698034 ◽

2012 ◽

Vol 2012 ◽

pp. 1-9 ◽

Cited By ~ 44

Author(s):

K. J. Rolfe ◽

A. O. Grobbelaar

Keyword(s):

Wound Healing ◽

Therapeutic Targets ◽

Complex Process ◽

New Therapeutic Targets ◽

Scarless Healing

Wound healing is a complex process involving a number of processes. Fetal regeneration has been shown to have a number of differences compared to scar-forming healing. This review discusses the number of differences identified in fetal regeneration. Understanding these differences may result in new therapeutic targets which may reduce or even prevent scarring in adult healing.

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ultrastructural process of intestinal wound healing

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100141494 ◽

1995 ◽

Vol 53 ◽

pp. 1024-1025

Author(s):

Rick L. Vaughn ◽

Shailendra K. Saxena ◽

John G. Sharp

Keyword(s):

Wound Healing ◽

Epithelial Cells ◽

Smooth Muscles ◽

Microscopic Level ◽

Light Microscopic Level ◽

Ileal Mucosa ◽

Wound Model ◽

Serosal Surface ◽

Complex Process ◽

Orderly Fashion

We have developed an intestinal wound model that includes surgical construction of an ileo-cecal patch to study the complex process of intestinal wound healing. This allows approximation of ileal mucosa to the cecal serosa and facilitates regeneration of ileal mucosa onto the serosal surface of the cecum. The regeneration of ileal mucosa can then be evaluated at different times. The wound model also allows us to determine the rate of intestinal regeneration for a known size of intestinal wound and can be compared in different situations (e.g. with and without EGF and Peyer’s patches).At the light microscopic level it appeared that epithelial cells involved in regeneration of ileal mucosa originated from the enlarged crypts adjacent to the intestinal wound and migrated in an orderly fashion onto the serosal surface of the cecum. The migrating epithelial cells later formed crypts and villi by the process of invagination and evagination respectively. There were also signs of proliferation of smooth muscles underneath the migratory epithelial cells.

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Healing gone wrong: convergence of hemostatic pathways and liver fibrosis?

Clinical Science ◽

10.1042/cs20191102 ◽

2020 ◽

Vol 134 (16) ◽

pp. 2189-2201

Author(s):

Jessica P.E. Davis ◽

Stephen H. Caldwell

Keyword(s):

Wound Healing ◽

Liver Disease ◽

Hepatic Fibrosis ◽

Cell Activation ◽

Stellate Cell ◽

Factor Xa ◽

Clinical Trial Data ◽

Chronic Liver ◽

Healing Response ◽

Wound Healing Response

Abstract Fibrosis results from a disordered wound healing response within the liver with activated hepatic stellate cells laying down dense, collagen-rich extracellular matrix that eventually restricts liver hepatic synthetic function and causes increased sinusoidal resistance. The end result of progressive fibrosis, cirrhosis, is associated with significant morbidity and mortality as well as tremendous economic burden. Fibrosis can be conceptualized as an aberrant wound healing response analogous to a chronic ankle sprain that is driven by chronic liver injury commonly over decades. Two unique aspects of hepatic fibrosis – the chronic nature of insult required and the liver’s unique ability to regenerate – give an opportunity for pharmacologic intervention to stop or slow the pace of fibrosis in patients early in the course of their liver disease. Two potential biologic mechanisms link together hemostasis and fibrosis: focal parenchymal extinction and direct stellate cell activation by thrombin and Factor Xa. Available translational research further supports the role of thrombosis in fibrosis. In this review, we will summarize what is known about the convergence of hemostatic changes and hepatic fibrosis in chronic liver disease and present current preclinical and clinical data exploring the relationship between the two. We will also present clinical trial data that underscores the potential use of anticoagulant therapy as an antifibrotic factor in liver disease.

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