Ca<sup>2+</sup> Signaling in Cardiovascular Fibroblasts

Fibrogenesis is a physiological process required for wound healing and tissue repair. It is induced by activation of quiescent fibroblasts, which first proliferate and then change their phenotype into migratory, contractile myofibroblasts. Myofibroblasts secrete extracellular matrix proteins, such a...

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Main Authors: Andreas Rinne, Florentina Pluteanu
Format: Article
Language:English
Published: MDPI AG 2024-10-01
Series:Biomolecules
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Online Access:https://www.mdpi.com/2218-273X/14/11/1365
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author Andreas Rinne
Florentina Pluteanu
author_facet Andreas Rinne
Florentina Pluteanu
author_sort Andreas Rinne
collection DOAJ
description Fibrogenesis is a physiological process required for wound healing and tissue repair. It is induced by activation of quiescent fibroblasts, which first proliferate and then change their phenotype into migratory, contractile myofibroblasts. Myofibroblasts secrete extracellular matrix proteins, such as collagen, to form a scar. Once the healing process is terminated, most myofibroblasts undergo apoptosis. However, in some tissues, such as the heart, myofibroblasts remain active and sensitive to neurohumoral factors and inflammatory mediators, which lead eventually to excessive organ fibrosis. Many cellular processes involved in fibroblast activation, including cell proliferation, protein secretion and cell contraction, are highly regulated by intracellular Ca<sup>2+</sup> signals. This review summarizes current research on Ca<sup>2+</sup> signaling pathways underlying fibroblast activation. We present receptor- and ion channel-mediated Ca<sup>2+</sup> signaling pathways, discuss how localized Ca<sup>2+</sup> signals of the cell nucleus may be involved in fibroblast activation and present Ca<sup>2+</sup>-sensitive transcription pathways relevant for fibroblast biology. When investigated, we highlight how the function of Ca<sup>2+</sup>-handling proteins changes during cardiac and pulmonary fibrosis. Many aspects of Ca<sup>2+</sup> signaling remain unexplored in different types of cardiovascular fibroblasts in relation to pathologies, and a better understanding of Ca<sup>2+</sup> signaling in fibroblasts will help to design targeted therapies against fibrosis.
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spelling doaj-art-e501c99ad95b4d8e9dd457165ab983ef2024-11-26T17:53:59ZengMDPI AGBiomolecules2218-273X2024-10-011411136510.3390/biom14111365Ca<sup>2+</sup> Signaling in Cardiovascular FibroblastsAndreas Rinne0Florentina Pluteanu1Department of Biophysics and Cellular Biotechnology, University of Medicine and Pharmacy “Carol Davila” Bucharest, 050474 Bucharest, RomaniaDepartment of Anatomy, Animal Physiology and Biophysics, Faculty of Biology, University of Bucharest, 050095 Bucharest, RomaniaFibrogenesis is a physiological process required for wound healing and tissue repair. It is induced by activation of quiescent fibroblasts, which first proliferate and then change their phenotype into migratory, contractile myofibroblasts. Myofibroblasts secrete extracellular matrix proteins, such as collagen, to form a scar. Once the healing process is terminated, most myofibroblasts undergo apoptosis. However, in some tissues, such as the heart, myofibroblasts remain active and sensitive to neurohumoral factors and inflammatory mediators, which lead eventually to excessive organ fibrosis. Many cellular processes involved in fibroblast activation, including cell proliferation, protein secretion and cell contraction, are highly regulated by intracellular Ca<sup>2+</sup> signals. This review summarizes current research on Ca<sup>2+</sup> signaling pathways underlying fibroblast activation. We present receptor- and ion channel-mediated Ca<sup>2+</sup> signaling pathways, discuss how localized Ca<sup>2+</sup> signals of the cell nucleus may be involved in fibroblast activation and present Ca<sup>2+</sup>-sensitive transcription pathways relevant for fibroblast biology. When investigated, we highlight how the function of Ca<sup>2+</sup>-handling proteins changes during cardiac and pulmonary fibrosis. Many aspects of Ca<sup>2+</sup> signaling remain unexplored in different types of cardiovascular fibroblasts in relation to pathologies, and a better understanding of Ca<sup>2+</sup> signaling in fibroblasts will help to design targeted therapies against fibrosis.https://www.mdpi.com/2218-273X/14/11/1365fibroblastmyofibroblastCa<sup>2+</sup> signalingcardiac fibrosispulmonary fibrosisCa<sup>2+</sup> ion channels
spellingShingle Andreas Rinne
Florentina Pluteanu
Ca<sup>2+</sup> Signaling in Cardiovascular Fibroblasts
Biomolecules
fibroblast
myofibroblast
Ca<sup>2+</sup> signaling
cardiac fibrosis
pulmonary fibrosis
Ca<sup>2+</sup> ion channels
title Ca<sup>2+</sup> Signaling in Cardiovascular Fibroblasts
title_full Ca<sup>2+</sup> Signaling in Cardiovascular Fibroblasts
title_fullStr Ca<sup>2+</sup> Signaling in Cardiovascular Fibroblasts
title_full_unstemmed Ca<sup>2+</sup> Signaling in Cardiovascular Fibroblasts
title_short Ca<sup>2+</sup> Signaling in Cardiovascular Fibroblasts
title_sort ca sup 2 sup signaling in cardiovascular fibroblasts
topic fibroblast
myofibroblast
Ca<sup>2+</sup> signaling
cardiac fibrosis
pulmonary fibrosis
Ca<sup>2+</sup> ion channels
url https://www.mdpi.com/2218-273X/14/11/1365
work_keys_str_mv AT andreasrinne casup2supsignalingincardiovascularfibroblasts
AT florentinapluteanu casup2supsignalingincardiovascularfibroblasts