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Editorial
. 2021 Jan 20:11:641771.
doi: 10.3389/fphys.2020.641771. eCollection 2020.

Editorial: Cardiac Fibrosis, From Lineage Tracing to Therapeutic Application

Claudio de Lucia  1 , Markus Wallner  2   3   4 , Domenico Corradi  5 , Gianluigi Pironti  6
Affiliations
Editorial

Editorial: Cardiac Fibrosis, From Lineage Tracing to Therapeutic Application

Claudio de Lucia et al. Front Physiol. .
No abstract available

Keywords: anti-fibrotic therapy; cardiac fibroblast; cardiac fibrosis; lineage tracing; myofibroblast; reactive fibrosis; reparative fibrosis.

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Conflict of interest statement

MW was employed by the company Center for Biomarker Research in Medicine, CBmed GmbH, Austria. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Cartoon depicting two pathogenic mechanisms of cardiac fibrosis, “reparative” (replacing dead cardiomyocytes) and “reactive” (interstitial and perivascular) cardiac fibrosis (blue color). Pro-fibrotic factors (TGF-β, AngII, PDGF, and CTGF) and cytokines released from inflammatory cells promote differentiation of fibroblasts toward activated myofibroblasts and matrifibrocytes actively producing extracellular matrix (ECM). Specific biomarkers of different stages of cardiac fibroblast differentiation are indicated on the bottom. TGF-β, transforming grow factor β; Ang II, angiotensin type II; PDGF, platelet derived grow factor; CTGF, connective tissue grow factor; Tcf21, transcription factor 21(biomarker for cardiac fibroblasts); Periostin, (biomarker of activated myofibroblasts) Acta2, smooth muscle actin alpha 2 (biomarker of matrifibrocytes); α-SMA, α smooth muscle actin.
See this image and copyright information in PMC

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  • Editorial on the Research Topic Cardiac Fibrosis, From Lineage Tracing to Therapeutic Application

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