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  4. Paracrine mechanism of redox signalling for post-mitotic cell and tissue regeneration
 
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Paracrine mechanism of redox signalling for post-mitotic cell and tissue regeneration
Author(s)
Hervera, A
Santos, CX
De Virgiliis, F
Shah, AM
Di Giovanni, Simone
Type
Journal Article
Abstract
Adult postmitotic mammalian cells, including neurons and cardiomyocytes, have a limited capacity to regenerate after injury. Therefore, an understanding of the molecular mechanisms underlying their regenerative ability is critical to advance tissue repair therapies. Recent studies highlight how redox signalling via paracrine cell-to-cell communication may act as a central mechanism coupling tissue injury with regeneration. Post-injury redox paracrine signalling can act by diffusion to nearby cells, through mitochondria or within extracellular vesicles, affecting specific intracellular targets such as kinases, phosphatases, and transcription factors, which in turn trigger a regenerative response. Here, we review redox paracrine signalling mechanisms in postmitotic tissue regeneration and discuss current challenges and future directions.
Date Issued
2019-06-01
Date Acceptance
2018-12-01
Citation
Trends in Cell Biology, 2019, 29 (6), pp.514-530
URI
http://hdl.handle.net/10044/1/69004
DOI
https://www.dx.doi.org/10.1016/j.tcb.2019.01.006
ISSN
0962-8924
Publisher
Elsevier
Start Page
514
End Page
530
Journal / Book Title
Trends in Cell Biology
Volume
29
Issue
6
Copyright Statement
© 2019 Published by Elsevier Ltd. This manuscript is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International Licence http://creativecommons.org/licenses/by-nc-nd/4.0/
Subjects
Science & Technology
Life Sciences & Biomedicine
Cell Biology
HYPOXIA-INDUCIBLE FACTOR-1-ALPHA
MITOCHONDRIAL COMPLEX-III
RETINAL GANGLION-CELLS
NADPH OXIDASE ACTIVITY
NF-KAPPA-B
AXONAL REGENERATION
HEART REGENERATION
OXIDATIVE STRESS
GROWTH-FACTOR
DEPENDENT ACTIVATION
06 Biological Sciences
11 Medical and Health Sciences
Developmental Biology
Publication Status
Published
Date Publish Online
2019-02-19
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