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      Mechanisms underlying pathological scarring by fibroblasts during wound healing

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          Abstract

          Pathological scarring is an abnormal outcome of wound healing, which often manifests as excessive proliferation and transdifferentiation of fibroblasts (FBs), and excessive deposition of the extracellular matrix. FBs are the most important effector cells involved in wound healing and scar formation. The factors that promote pathological scar formation often act on the proliferation and function of FB. In this study, we describe the factors that lead to abnormal FB formation in pathological scarring in terms of the microenvironment, signalling pathways, epigenetics, and autophagy. These findings suggest that understanding the causes of abnormal FB formation may aid in the development of precise and effective preventive and treatment strategies for pathological scarring that are associated with improved quality of life of patients.

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          Regulation of chromatin by histone modifications.

          Andrew Bannister, Tony Kouzarides (2011)
          Chromatin is not an inert structure, but rather an instructive DNA scaffold that can respond to external cues to regulate the many uses of DNA. A principle component of chromatin that plays a key role in this regulation is the modification of histones. There is an ever-growing list of these modifications and the complexity of their action is only just beginning to be understood. However, it is clear that histone modifications play fundamental roles in most biological processes that are involved in the manipulation and expression of DNA. Here, we describe the known histone modifications, define where they are found genomically and discuss some of their functional consequences, concentrating mostly on transcription where the majority of characterisation has taken place.
          Article 0 comments Cited 987 times – based on 0 reviews     Review now
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            Wound healing: cellular mechanisms and pathological outcomes

            Holly Wilkinson, Matthew J. Hardman (2020)
            Wound healing is a complex, dynamic process supported by a myriad of cellular events that must be tightly coordinated to efficiently repair damaged tissue. Derangement in wound-linked cellular behaviours, as occurs with diabetes and ageing, can lead to healing impairment and the formation of chronic, non-healing wounds. These wounds are a significant socioeconomic burden due to their high prevalence and recurrence. Thus, there is an urgent requirement for the improved biological and clinical understanding of the mechanisms that underpin wound repair. Here, we review the cellular basis of tissue repair and discuss how current and emerging understanding of wound pathology could inform future development of efficacious wound therapies.
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              Keloid and Hypertrophic Scars Are the Result of Chronic Inflammation in the Reticular Dermis

              Rei Ogawa (2017)
              Keloids and hypertrophic scars are caused by cutaneous injury and irritation, including trauma, insect bite, burn, surgery, vaccination, skin piercing, acne, folliculitis, chicken pox, and herpes zoster infection. Notably, superficial injuries that do not reach the reticular dermis never cause keloidal and hypertrophic scarring. This suggests that these pathological scars are due to injury to this skin layer and the subsequent aberrant wound healing therein. The latter is characterized by continuous and histologically localized inflammation. As a result, the reticular layer of keloids and hypertrophic scars contains inflammatory cells, increased numbers of fibroblasts, newly formed blood vessels, and collagen deposits. Moreover, proinflammatory factors, such as interleukin (IL)-1α, IL-1β, IL-6, and tumor necrosis factor-α are upregulated in keloid tissues, which suggests that, in patients with keloids, proinflammatory genes in the skin are sensitive to trauma. This may promote chronic inflammation, which in turn may cause the invasive growth of keloids. In addition, the upregulation of proinflammatory factors in pathological scars suggests that, rather than being skin tumors, keloids and hypertrophic scars are inflammatory disorders of skin, specifically inflammatory disorders of the reticular dermis. Various external and internal post-wounding stimuli may promote reticular inflammation. The nature of these stimuli most likely shapes the characteristics, quantity, and course of keloids and hypertrophic scars. Specifically, it is likely that the intensity, frequency, and duration of these stimuli determine how quickly the scars appear, the direction and speed of growth, and the intensity of symptoms. These proinflammatory stimuli include a variety of local, systemic, and genetic factors. These observations together suggest that the clinical differences between keloids and hypertrophic scars merely reflect differences in the intensity, frequency, and duration of the inflammation of the reticular dermis. At present, physicians cannot (or at least find it very difficult to) control systemic and genetic risk factors of keloids and hypertrophic scars. However, they can use a number of treatment modalities that all, interestingly, act by reducing inflammation. They include corticosteroid injection/tape/ointment, radiotherapy, cryotherapy, compression therapy, stabilization therapy, 5-fluorouracil (5-FU) therapy, and surgical methods that reduce skin tension.
              Article 0 comments Cited 271 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Suling Xu: xusuling@nbu.edu.cn
                Journal
                Journal ID (nlm-ta): Int Wound J
                Journal ID (iso-abbrev): Int Wound J
                Journal ID (doi): 10.1111/(ISSN)1742-481X
                Journal ID (publisher-id): IWJ
                Title: International Wound Journal
                Publisher: Blackwell Publishing Ltd (Oxford, UK )
                ISSN (Print): 1742-4801
                ISSN (Electronic): 1742-481X
                Publication date (Electronic): 01 February 2023
                Publication date Collection: August 2023
                Volume: 20
                Issue: 6 ( doiID: 10.1111/iwj.v20.6 )
                Pages: 2190-2206
                Affiliations
                [ 1 ] The Affiliated Hospital of Medical School Ningbo University Ningbo China
                Author notes
                [*] [* ] Correspondence

                Suling Xu, The The Affiliated Hospital of Medical School, Ningbo University, Ningbo 315020, China.

                Email: xusuling@ 123456nbu.edu.cn

                Article
                Publisher ID: IWJ14097
                DOI: 10.1111/iwj.14097
                PMC ID: 10333014
                PubMed ID: 36726192
                SO-VID: d5ab1e12-71ea-4c0b-879c-6ec4ee751aaf
                Copyright © © 2023 The Authors. International Wound Journal published by Medicalhelplines.com Inc and John Wiley & Sons Ltd.
                License:

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

                History
                Date received : 08 November 2022
                Date accepted : 09 January 2023
                Page count
                Figures: 1, Tables: 1, Pages: 17, Words: 10681
                Funding
                Funded by: Major Science and Technology Program for Medicine and Health in Zhejiang Province
                Award ID: WKJ‐ZJ‐2012
                Funded by: the Public Welfare Projects of Ningbo, China
                Award ID: 2022S065
                Categories
                Subject: Original Article
                Subject: Original Articles
                Custom metadata
                source-schema-version-number 2.0
                cover-date August 2023
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_JATSPMC version:6.3.1 mode:remove_FC converted:10.07.2023

                ScienceOpen disciplines: Emergency medicine & Trauma
                Keywords: fibroblasts,fibrosis,keloid,scar,wound healing
                Data availability:
                ScienceOpen disciplines: Emergency medicine & Trauma
                Keywords: fibroblasts, fibrosis, keloid, scar, wound healing

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