Interleukin-11 signaling promotes cellular reprogramming and limits fibrotic scarring during tissue regeneration-Reference-Cited by-同舟云学术

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

Published:2021-09-10 Issue:37 Volume:7 Page:
ISSN:2375-2548
Container-title:Science Advances
language:en
Short-container-title:Sci. Adv.

Author:

Allanki Srinivas¹²³^ORCID,Strilic Boris⁴,Scheinberger Lilly¹,Onderwater Yeszamin L.¹^ORCID,Marks Alora¹,Günther Stefan⁵^ORCID,Preussner Jens²⁶^ORCID,Kikhi Khrievono⁷^ORCID,Looso Mario²⁶^ORCID,Stainier Didier Y. R.¹²⁸^ORCID,Reischauer Sven¹³⁸^ORCID

Affiliation:

1. Department of Developmental Genetics, Max Planck Institute for Heart and Lung Research, 61231 Bad Nauheim, Germany.

2. German Centre for Cardiovascular Research (DZHK), Partner Site Rhine-Main, 60596 Frankfurt am Main, Germany.

3. Medical Clinic I (Cardiology/Angiology) and Campus Kerckhoff, Justus-Liebig-University Giessen, 35392 Giessen, Germany.

4. Department of Pharmacology, Max Planck Institute for Heart and Lung Research, 61231 Bad Nauheim, Germany.

5. Bioinformatics and Deep Sequencing Platform, Max Planck Institute for Heart and Lung Research, 61231 Bad Nauheim, Germany.

6. Bioinformatics Core Unit (BCU), Max Planck Institute for Heart and Lung Research, 61231 Bad Nauheim, Germany.

7. Flow Cytometry Service Group, Max Planck Institute for Heart and Lung Research, 61231 Bad Nauheim, Germany.

8. Cardio-Pulmonary Institute, Frankfurt, Germany.

Abstract

The cytokine interleukin-11 promotes regeneration and limits scar formation in multiple zebrafish tissues after injury.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

Reference80 articles.

1. Wound repair and regeneration

2. Myofibroblasts: Trust your heart and let fate decide

3. Specialized fibroblast differentiated states underlie scar formation in the infarcted mouse heart

4. Experimental myocardial infarction triggers canonical Wnt signaling and endothelial-to-mesenchymal transition

5. Macrophages promote endothelial-to-mesenchymal transition via MT1-MMP/TGFβ1 after myocardial infarction

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