Document Type

Article

Publication Date

6-6-2023

Comments

This article is the author's final published version in Biomolecules, Volume 13, Issue 6, June 2023, Article number 945.

The published version is available at https://doi.org/10.3390/biom13060945.

Copyright © 2023 by the author. Licensee MDPI, Basel, Switzerland.

This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https:// creativecommons.org/licenses/by/ 4.0/).

Abstract

Wound healing is triggered by inflammation elicited after tissue injury. Mesenchymal cells, specifically fibroblasts, accumulate in the injured tissues, where they engage in tissue repair through the expression and assembly of extracellular matrices that provide a scaffold for cell adhesion, the re-epithelialization of tissues, the production of soluble bioactive mediators that promote cellular recruitment and differentiation, and the regulation of immune responses. If appropriately deployed, these processes promote adaptive repair, resulting in the preservation of the tissue structure and function. Conversely, the dysregulation of these processes leads to maladaptive repair or disrepair, which causes tissue destruction and a loss of organ function. Thus, fibroblasts not only serve as structural cells that maintain tissue integrity, but are key effector cells in the process of wound healing. The review will discuss the general concepts about the origins and heterogeneity of this cell population and highlight the specific fibroblast functions disrupted in human disease. Finally, the review will explore the role of fibroblasts in tissue disrepair, with special attention to the lung, the role of aging, and how alterations in the fibroblast phenotype underpin disorders characterized by pulmonary fibrosis.

Creative Commons License

Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.

PubMed ID

37371525

Language

English

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