Abstract
Fibroblasts are the chief effector cells in fibrotic diseases and have been discovered to be highly heterogeneous. Recently, fibroblast heterogeneity in human skin has been studied extensively and several surface markers for dermal fibroblast subtypes have been identified, holding promise for future antifibrotic therapies. However, it has yet to be confirmed whether surface markers should be looked upon as merely lineage landmarks or as functional entities of fibroblast subtypes, which may further complicate the interpretation of cellular function of these fibroblast subtypes. This review aims to provide an update on current evidence on fibroblast surface markers in fibrotic disorders of skin as well as of other organ systems. Specifically, studies where surface markers were treated as lineage markers and manipulated as functional membrane proteins are both evaluated in parallel, hoping to reveal the underlying mechanism behind the pathogenesis of tissue fibrosis contributed by various fibroblast subtypes from multiple angles, shedding lights on future translational researches.
Highlights
Fibroblast (Fb), as a vital interstitial cell, is involved in a wide variety of biological functions such as conferring structural support to tissues, secreting extracellular matrix (ECM), participating in tissue damage repair and immune responses (Lynch and Watt, 2018)
A more comprehensive transcriptomic, proteomic or genome-wide epigenetic profiling of Fb subtypes defined by different surface markers would be instrumental for a more in-depth understanding of the evolution and functional characteristics of each Fb subtype in tissue fibrosis
All authors wrote and approved the final manuscript
Summary
Fibroblast (Fb), as a vital interstitial cell, is involved in a wide variety of biological functions such as conferring structural support to tissues, secreting extracellular matrix (ECM), participating in tissue damage repair and immune responses (Lynch and Watt, 2018). Based on currently available evidence, it is acknowledged that pan-Fb surface markers of human skin Fb are CD90, PDGFR α and PDGFRβ, while the surface markers of Fb subtypes are FAP, CD26, CD36, and CD39. These surface markers hold the promise of future antifibrotic therapies by targeting Fb subtypes with small molecule inhibitors or inhibitory antibodies. Antifibrotic therapies targeting certain Fb subtypes or particular surface marker proteins would be evaluated, hoping to shed light on the significance of these Fb subtypes during the fibrotic process, and to provide some valuable insights for future translational research
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