Format

Send to

Choose Destination
J Mol Cell Cardiol. 2016 Apr;93:143-8. doi: 10.1016/j.yjmcc.2015.11.016. Epub 2015 Nov 20.

Role of inflammatory cells in fibroblast activation.

Author information

1
Center for Cardiovascular Research, Division of Cardiology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, United States.
2
Center for Cardiovascular Research, Division of Cardiology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, United States. Electronic address: dmann@dom.wustl.edu.

Abstract

Although fibrosis is an essential response to acute cardiac tissue injury, prolonged myofibroblast activation and progressive fibrosis lead to further distortion of tissue architecture and worsened cardiac function. Thus, optimal tissue repair following injury requires tight control over myofibroblast activation. It is now recognized that inflammation plays a critical role in regulating fibrosis. In this review we will highlight how advances in the field of innate immunity have led to a better understanding of the role of inflammation in cardiovascular disease and, in particular, in the regulation of fibrosis. Specifically, we will discuss how the innate immune system recognizes tissue damage in settings of acute injury and chronic cardiovascular disease. We will also review the role of different cell populations in this response, particularly the unique role of different macrophage subsets and mast cells.

KEYWORDS:

Fibrosis; Inflammation; Innate immunity; Macrophage; Mast cell

PMID:
26593723
PMCID:
PMC4846511
DOI:
10.1016/j.yjmcc.2015.11.016
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center