Next Article in Journal / Special Issue
The Non-Fibrillar Side of Fibrosis: Contribution of the Basement Membrane, Proteoglycans, and Glycoproteins to Myocardial Fibrosis
Previous Article in Journal
Arterial Structural and Functional Characteristics at End of Early Childhood and Beginning of Adulthood: Impact of Body Size Gain during Early, Intermediate, Late and Global Growth
Previous Article in Special Issue
Cardiac Fibroblasts and the Extracellular Matrix in Regenerative and Nonregenerative Hearts
Open AccessReview

Ca2+ Signaling in Cardiac Fibroblasts and Fibrosis-Associated Heart Diseases

Calhoun Cardiology Center, Department of Cell Biology, University of Connecticut Health Center, Farmington, CT 06030, USA
Department of Pharmacology, Rutgers, Robert Wood Johnson Medical School, Piscataway, NJ 08854, USA
Authors to whom correspondence should be addressed.
J. Cardiovasc. Dev. Dis. 2019, 6(4), 34;
Received: 11 August 2019 / Revised: 16 September 2019 / Accepted: 18 September 2019 / Published: 23 September 2019
(This article belongs to the Special Issue Cardiac Fibroblasts and Fibrosis)
Cardiac fibrosis is the excessive deposition of extracellular matrix proteins by cardiac fibroblasts and myofibroblasts, and is a hallmark feature of most heart diseases, including arrhythmia, hypertrophy, and heart failure. This maladaptive process occurs in response to a variety of stimuli, including myocardial injury, inflammation, and mechanical overload. There are multiple signaling pathways and various cell types that influence the fibrogenesis cascade. Fibroblasts and myofibroblasts are central effectors. Although it is clear that Ca2+ signaling plays a vital role in this pathological process, what contributes to Ca2+ signaling in fibroblasts and myofibroblasts is still not wholly understood, chiefly because of the large and diverse number of receptors, transporters, and ion channels that influence intracellular Ca2+ signaling. Intracellular Ca2+ signals are generated by Ca2+ release from intracellular Ca2+ stores and by Ca2+ entry through a multitude of Ca2+-permeable ion channels in the plasma membrane. Over the past decade, the transient receptor potential (TRP) channels have emerged as one of the most important families of ion channels mediating Ca2+ signaling in cardiac fibroblasts. TRP channels are a superfamily of non-voltage-gated, Ca2+-permeable non-selective cation channels. Their ability to respond to various stimulating cues makes TRP channels effective sensors of the many different pathophysiological events that stimulate cardiac fibrogenesis. This review focuses on the mechanisms of Ca2+ signaling in fibroblast differentiation and fibrosis-associated heart diseases and will highlight recent advances in the understanding of the roles that TRP and other Ca2+-permeable channels play in cardiac fibrosis. View Full-Text
Keywords: Ca2+ signaling pathways; TRP channels; cardiac fibroblasts; cardiac fibrosis; ion channels Ca2+ signaling pathways; TRP channels; cardiac fibroblasts; cardiac fibrosis; ion channels
Show Figures

Figure 1

MDPI and ACS Style

Feng, J.; Armillei, M.K.; Yu, A.S.; Liang, B.T.; Runnels, L.W.; Yue, L. Ca2+ Signaling in Cardiac Fibroblasts and Fibrosis-Associated Heart Diseases. J. Cardiovasc. Dev. Dis. 2019, 6, 34.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

Search more from Scilit
Back to TopTop