Dynamic Involvement of Telocytes in Modulating Multiple Signaling Pathways in Cardiac Cytoarchitecture

Cardiac interstitium is a complex and dynamic environment, vital for normal cardiac structure and function. Telocytes are active cellular players in regulating main events that feature myocardial homeostasis and orchestrating its involvement in heart pathology. Despite the great amount of data sugge...

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Bibliographic Details
Published in:International journal of molecular sciences 2022-05, Vol.23 (10), p.5769
Main Authors: Cucu, Ioana, Nicolescu, Mihnea Ioan, Busnatu, Ștefan-Sebastian, Manole, Cătălin Gabriel
Format: Article
Language:English
Subjects:
1-Phosphatidylinositol 3-kinase
AKT protein
Apoptosis
Cardiomyocytes
Cell cycle
Cellular structure
Extracellular matrix
Gene expression
Genomics
Heart
heart failure
Homeostasis
Kinases
Ligands
MicroRNAs
PI3K/AKT
Proteins
Review
Scanning electron microscopy
Signal transduction
Structure-function relationships
telocytes
TGFB
Transmission electron microscopy
Vascular endothelial growth factor
WNT
Wnt protein
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Summary:Cardiac interstitium is a complex and dynamic environment, vital for normal cardiac structure and function. Telocytes are active cellular players in regulating main events that feature myocardial homeostasis and orchestrating its involvement in heart pathology. Despite the great amount of data suggesting (microscopically, proteomically, genetically, etc.) the implications of telocytes in the different physiological and reparatory/regenerative processes of the heart, understanding their involvement in realizing the heart's mature cytoarchitecture is still at its dawn. Our scrutiny of the recent literature gave clearer insights into the implications of telocytes in the WNT signaling pathway, but also TGFB and PI3K/AKT pathways that, inter alia, conduct cardiomyocytes differentiation, maturation and final integration into heart adult architecture. These data also strengthen evidence for telocytes as promising candidates for cellular therapies in various heart pathologies.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms23105769