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  Interleukin-11 signaling promotes cellular reprogramming and limits fibrotic scarring during tissue regeneration

Allanki, S., Strilic, B., Scheinberger, L., Onderwater, Y. L., Marks, A., Guenther, S., et al. (2021). Interleukin-11 signaling promotes cellular reprogramming and limits fibrotic scarring during tissue regeneration. SCIENCE ADVANCES, 7(37): eabg6497. doi:10.1126/sciadv.abg6497.

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 Creators:
Allanki, Srinivas1, Author              
Strilic, Boris2, Author              
Scheinberger, Lilly, Author
Onderwater, Yeszamin L., Author
Marks, Alora1, Author              
Guenther, Stefan3, Author              
Preussner, Jens4, Author              
Kikhi, Khrievono1, Author              
Looso, Mario4, Author              
Stainier, Didier Y. R.1, Author              
Reischauer, Sven1, Author              
Affiliations:
1Developmental Genetics, Max Planck Institute for Heart and Lung Research, Max Planck Society, ou_2591697              
2Pharmacology, Max Planck Institute for Heart and Lung Research, Max Planck Society, ou_2591696              
3Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, Max Planck Society, ou_2591695              
4Bioinformatics, Max Planck Institute for Heart and Lung Research, Max Planck Society, ou_2591704              

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Free keywords: HEART REGENERATION; TARGETED DISRUPTION; BLASTEMA FORMATION; EPICARDIAL CELLS; IN-VIVO; ZEBRAFISH; INJURY; IL-11; DEDIFFERENTIATION; TRANSDUCERScience & Technology - Other Topics;
 Abstract: Damage-induced fibrotic scarring limits tissue regeneration in mammals and is a leading cause of morbidity. In contrast, species like zebrafish can regenerate damaged tissues without excessive fibrosis. However, whether specific signaling pathways can both limit fibrosis and promote regeneration is unclear. Here, we show that interleukin-11 (Il-11)/Stat3 signaling has such a dual function. Zebrafish lacking Il-11 receptor function display severely compromised heart, fin, and scale regeneration. Deep phenotyping and transcriptional analysis of adult hearts and fins show that Il-11 signaling drives cellular reprogramming to orchestrate global and tissue-specific regenerative programs and broadly antagonizes hallmarks of adult mammalian scarring. Mechanistically, our data indicate that IL-11 signaling in endothelial cells antagonizes profibrotic transforming growth factor-beta signaling and endothelial-to-mesenchymal transition, limiting scarring and promoting cardiomyocyte repopulation, after injury. Overall, our findings position damage-induced Il-11/Stat3 signaling in a key role limiting fibrosis and promoting regeneration, revealing novel targets for regenerative therapies.

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Language(s): eng - English
 Dates: 2021-09-08
 Publication Status: Published online
 Pages: 18
 Publishing info: -
 Table of Contents: -
 Rev. Type: -
 Identifiers: ISI: 000695713400004
DOI: 10.1126/sciadv.abg6497
PMID: 34516874
 Degree: -

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Title: SCIENCE ADVANCES
Source Genre: Journal
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Publ. Info: 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA : AMER ASSOC ADVANCEMENT SCIENCE
Pages: - Volume / Issue: 7 (37) Sequence Number: eabg6497 Start / End Page: - Identifier: ISSN: 2375-2548