Liver-heart cross-talk mediated by coagulation factor XI protects against heart failure-Reference-Cited by-同舟云学术

Liver-heart cross-talk mediated by coagulation factor XI protects against heart failure

Published:2022-09-23 Issue:6613 Volume:377 Page:1399-1406
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Cao Yang¹^ORCID,Wang Yuchen¹,Zhou Zhenqi²^ORCID,Pan Calvin¹^ORCID,Jiang Ling³^ORCID,Zhou Zhiqiang¹,Meng Yonghong¹,Charugundla Sarada¹,Li Tao³^ORCID,Allayee Hooman⁴^ORCID,Seldin Marcus M.⁵,Lusis Aldons J.¹⁶⁷^ORCID

Affiliation:

1. Department of Medicine, Division of Cardiology, University of California, Los Angeles, CA 90095, USA.

2. Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, University of California, Los Angeles, CA 90095, USA.

3. Department of Anesthesiology, Laboratory of Mitochondria and Metabolism, West China Hospital of Sichuan University, Chengdu 610041, China.

4. Departments of Population and Public Health Sciences and Biochemistry and Molecular Medicine, University of Southern California Keck School of Medicine, Los Angeles, CA 90089, USA.

5. Department of Biological Chemistry and Center for Epigenetics and Metabolism, University of California, Irvine School of Medicine, Irvine, CA 92697, USA.

6. Department of Human Genetics, University of California, Los Angeles, CA 90095, USA.

7. Department of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, CA 90095, USA.

Abstract

Tissue-tissue communication by endocrine factors is a vital mechanism for physiologic homeostasis. A systems genetics analysis of transcriptomic and functional data from a cohort of diverse, inbred strains of mice predicted that coagulation factor XI (FXI), a liver-derived protein, protects against diastolic dysfunction, a key trait of heart failure with preserved ejection fraction. This was confirmed using gain- and loss-of-function studies, and FXI was found to activate the bone morphogenetic protein (BMP)–SMAD1/5 pathway in the heart. The proteolytic activity of FXI is required for the cleavage and activation of extracellular matrix–associated BMP7 in the heart, thus inhibiting genes involved in inflammation and fibrosis. Our results reveal a protective role of FXI in heart injury that is distinct from its role in coagulation.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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