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

Yang Cao | Zendy; Yuchen Wang | Zendy; Zhenqi Zhou | Zendy; Calvin Pan | Zendy; Ling Jiang | Zendy; Zhiqiang Zhou | Zendy; Yonghong Meng | Zendy; Sarada Charugundla | Zendy; Tao Li | Zendy; Hooman Allayee | Zendy; Marcus M. Seldin | Zendy; Aldons J. Lusis | Zendy

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

Author(s) -

Yang Cao,

Yuchen Wang,

Zhenqi Zhou,

Calvin Pan,

Ling Jiang,

Zhiqiang Zhou,

Yonghong Meng,

Sarada Charugundla,

Tao Li,

Hooman Allayee,

Marcus M. Seldin,

Aldons J. Lusis

Publication year - 2022

Publication title -

science

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 12.556

H-Index - 1186

eISSN - 1095-9203

pISSN - 0036-8075

DOI - 10.1126/science.abn0910

Subject(s) - heart failure , coagulation , biology , homeostasis , medicine , endocrinology

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.

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