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      The Roles of Inflammation in Keloid and Hypertrophic Scars

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          Abstract

          The underlying mechanisms of wound healing are complex but inflammation is one of the determining factors. Besides its traditional role in combating against infection upon injury, the characteristics and magnitude of inflammation have dramatic impacts on the pathogenesis of scar. Keloids and hypertrophic scars are pathological scars that result from aberrant wound healing. They are characterized by continuous local inflammation and excessive collagen deposition. In this review, we aim at discussing how dysregulated inflammation contributes to the pathogenesis of scar formation. Immune cells, soluble inflammatory mediators, and the related intracellular signal transduction pathways are our three subtopics encompassing the events occurring in inflammation associated with scar formation. In the end, we enumerate the current and potential medicines and therapeutics for suppressing inflammation and limiting progression to scar. Understanding the initiation, progression, and resolution of inflammation will provide insights into the mechanisms of scar formation and is useful for developing effective treatments.

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          Most cited references76

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          Wound Healing: A Cellular Perspective

          Wound healing is one of the most complex processes in the human body. It involves the spatial and temporal synchronization of a variety of cell types with distinct roles in the phases of hemostasis, inflammation, growth, re-epithelialization, and remodeling. With the evolution of single cell technologies, it has been possible to uncover phenotypic and functional heterogeneity within several of these cell types. There have also been discoveries of rare, stem cell subsets within the skin, which are unipotent in the uninjured state, but become multipotent following skin injury. Unraveling the roles of each of these cell types and their interactions with each other is important in understanding the mechanisms of normal wound closure. Changes in the microenvironment including alterations in mechanical forces, oxygen levels, chemokines, extracellular matrix and growth factor synthesis directly impact cellular recruitment and activation, leading to impaired states of wound healing. Single cell technologies can be used to decipher these cellular alterations in diseased states such as in chronic wounds and hypertrophic scarring so that effective therapeutic solutions for healing wounds can be developed.
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            Fibrotic disease and the T(H)1/T(H)2 paradigm.

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              PAMP s and DAMP s: signal 0s that spur autophagy and immunity

              Summary Pathogen‐associated molecular pattern molecules (PAMPs) are derived from microorganisms and recognized by pattern recognition receptor (PRR)‐bearing cells of the innate immune system as well as many epithelial cells. In contrast, damage‐associated molecular pattern molecules (DAMPs) are cell‐derived and initiate and perpetuate immunity in response to trauma, ischemia, and tissue damage, either in the absence or presence of pathogenic infection. Most PAMPs and DAMPs serve as so‐called ‘Signal 0s’ that bind specific receptors [Toll‐like receptors, NOD‐like receptors, RIG‐I‐like receptors, AIM2‐like receptors, and the receptor for advanced glycation end products (RAGE)] to promote autophagy. Autophagy, a conserved lysosomal degradation pathway, is a cell survival mechanism invoked in response to environmental and cellular stress. Autophagy is inferred to have been present in the last common eukaryotic ancestor and only to have been lost by some obligatory intracellular parasites. As such, autophagy represents a unifying biology, subserving survival and the earliest host defense strategies, predating apoptosis, within eukaryotes. Here, we review recent advances in our understanding of autophagic molecular mechanisms and functions in emergent immunity.
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                Author and article information

                Contributors
                Journal
                Front Immunol
                Front Immunol
                Front. Immunol.
                Frontiers in Immunology
                Frontiers Media S.A.
                1664-3224
                04 December 2020
                2020
                : 11
                : 603187
                Affiliations
                [1] 1Department of Plastic Surgery, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine , Hangzhou, China
                [2] 2Department of Physiology, Zhejiang University School of Medicine , Hangzhou, China
                [3] 3Department of Cardiology of the Second Affiliated Hospital, and Institute of Translational Medicine, Zhejiang University School of Medicine , Hangzhou, China
                Author notes

                Edited by: Allison Cowin, University of South Australia, Australia

                Reviewed by: Andrew William Stevenson, University of Western Australia, Australia; Zlatko Kopecki, University of South Australia, Australia

                *Correspondence: Wei-Qiang Tan, tanweixxxx@ 123456zju.edu.cn ; Xiao Z. Shen, shenx@ 123456zju.edu.cn

                This article was submitted to Inflammation, a section of the journal Frontiers in Immunology

                Article
                10.3389/fimmu.2020.603187
                7746641
                33343575
                4469078e-dc09-4f35-ace3-01fcf8d4f344
                Copyright © 2020 Wang, Zhao, Cao, Liu, Sun, Shi, Cai, Shen and Tan

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 05 September 2020
                : 06 November 2020
                Page count
                Figures: 3, Tables: 0, Equations: 0, References: 77, Pages: 10, Words: 5315
                Funding
                Funded by: National Natural Science Foundation of China 10.13039/501100001809
                Award ID: 31970898, 81670378, 81700365, 31771266, 81701911, 81671918
                Categories
                Immunology
                Review

                Immunology
                immune cells,inflammatory mediators,signal transduction pathways,keloid,potential therapeutics,hypertrophic scar

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