Imperial College London
Alternate

ProfessorStuartCook

Faculty of Medicine, Institute of Clinical Sciences

Visiting Professor
 
 
 
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Contact

 

+44 (0)20 3313 1346stuart.cook

 
 
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Location

 

RF 16Sydney StreetRoyal Brompton Campus

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Summary

 

Publications

Citation

BibTex format

@article{Cook:2023:10.1007/s12265-022-10351-9,
author = {Cook, SA},
doi = {10.1007/s12265-022-10351-9},
journal = {Journal of Cardiovascular Translational Research},
pages = {755--757},
title = {The pathobiology of interleukin 11 in mammalian disease is likely explained by its essential evolutionary role for Fin regeneration},
url = {http://dx.doi.org/10.1007/s12265-022-10351-9},
volume = {16},
year = {2023}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Recent studies have shown IL11 to be pro-fibrotic, pro-inflammatory and anti-regenerative in heart, liver, lung and kidney disease in mice and humans. However, data also show that IL11 is specifically required for appendage regeneration following trauma in some species. In fish, tadpoles and axolotl, IL11 is uniquely upregulated in the regenerative organ, the blastema, following loss of fin, tail or limb. In this short essay I suggest that the pathobiology of IL11 in mammals is rooted in its deep evolutionary role for epimorphic appendage regeneration. In both blastema formation and mammalian disease there is robust IL11-driven fibroblast activation, extracellular matrix production, inflammation and epithelial cell dedifferentiation. While these cellular processes are critical for regeneration in lower species they cause organ failure in mammals. This hypothesis, if correct, may explain the apparent redundancy of IL11 for human health and suggest IL11 as a therapeutic target.
AU  - Cook,SA
DO  - 10.1007/s12265-022-10351-9
EP  - 757
PY  - 2023///
SN  - 1937-5395
SP  - 755
TI  - The pathobiology of interleukin 11 in mammalian disease is likely explained by its essential evolutionary role for Fin regeneration
T2  - Journal of Cardiovascular Translational Research
UR  - http://dx.doi.org/10.1007/s12265-022-10351-9
UR  - https://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000912205300001&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=a2bf6146997ec60c407a63945d4e92bb
UR  - https://link.springer.com/article/10.1007/s12265-022-10351-9
UR  - http://hdl.handle.net/10044/1/103119
VL  - 16
ER  -
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