Adipocytic Progenitor Cells Give Rise to Pathogenic Myofibroblasts: Adipocyte-to-Mesenchymal Transition and Its Emerging
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SCLERODERMA (J VARGA, SECTION EDITOR)
Adipocytic Progenitor Cells Give Rise to Pathogenic Myofibroblasts: Adipocyte-to-Mesenchymal Transition and Its Emerging Role in Fibrosis in Multiple Organs Roberta Goncalves Marangoni 1
&
Benjamin Korman 1 & John Varga 2
# Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Purpose of Review Adipocytes have recently been shown to be able to reprogram to a myofibroblastic phenotype in a process termed adipocyte mesenchymal transition (AMT). This review seeks to discuss the relevance of this process to disease and explore its mechanisms. Recent Findings AMT occurs in multiple organs and diseases, transdifferentiation goes through a precursor cell and there is a reversible process that can be influenced by metabolic stress, myeloid cells, immune dysregulation, and pharmacological intervention. Summary AMT is a newly appreciated and highly relevant process in multiple forms of fibrosis. Targeting AMT may serve as a novel method of treating fibrosis. Keywords Fibroblast . Myofibroblast . Adipocyte . Fibrosis . Scleroderma . Adipose mesenchymal transition
Introduction Fibroblasts and myofibroblasts are tissue-resident mesenchymal cells that serve as the main effectors in all forms of fibrosis, contributing to excessive scarring and organ dysfunction in a diverse group of chronic conditions [1]. Given their central role, fibroblasts and myofibroblasts have for two decades been the primary focus of studies seeking to understand the pathogenesis of fibrosis and the development of targeted anti-
fibrotic therapies. In this review, we will summarize recent progress regarding the cellular origins of fibroblasts in fibrotic states, and emerging evidence implicating a novel mechanism of adipocyte-derived myofibroblast differentiation as an important and therapeutically tractable mechanism in fibrosis in systemic sclerosis (SSc) and other diseases associated with fibrosis.
Fibroblasts and Myofibroblasts This article is part of the Topical Collection on Scleroderma * Roberta Goncalves Marangoni [email protected] Benjamin Korman [email protected] John Varga [email protected] 1
Division of Allergy, Immunology and Rheumatology, University of Rochester Medical Center, 601 Elmwood Avenue BOX 695, Rochester, NY 14642, USA
2
Division of Rheumatology, Northwestern University Feinberg School of Medicine, 240 E. Huron Street, McGaw Pavilion M-300, Chicago, IL 60611, USA
Fibroblasts are a heterogeneous group of tissue-resident mesenchymal cells. Fibroblasts produce collagen, are not terminally differentiated, and, significantly, lack uniform cell surface markers [2]. Multiple factors have been identified as triggers for fibroblast activation and important in disease pathogenesis. These include transforming growth factor-β (TGF-β), IL-11, platelet-derived growth factor (PDGF), Wnt, hedgehog, and YAP-TAZ signaling [3]. When activated, fibroblasts undergo extensive reprogramming and transition to a myofibroblast phenoty
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