Key result
Ischemia-induced liver responses mitigate myocardial infarction via hepatic cell mobilization and upregulation of FGF21 and TFF3.
Why the study?
Myocardial ischemia activates innate cardioprotective mechanisms, but the role of liver-mediated responses in myocardial protection was newly recognized and needed review.
Answers are grounded in this paper and cite their sources.
No immediate clinical implications for MI care; hypothesis-generating for liver-mediated protection requiring prospective validation.
Myocardial ischemia activates innate cardioprotective mechanisms, including expression of growth factors, activation of cardiac resident stem cells and mobilization of bone marrow cells to the ischemic myocardium, which alleviate ischemic injury and promote cardiomyocyte regeneration. This review addresses a newly recognized cardioprotective mechanism involving the liver. Myocardial ischemia induces liver responses, including mobilization of hepatic cells to the circulatory system and upregulation of hepatic secretory proteins, such as fibroblast growth factor 21 (FGF21) and trefoil factor 3 (TFF3). The mobilized hepatic cells either engraft to the ischemic myocardium or disintegrate in the circulatory system, facilitating delivery of the hepatic secretory proteins. These proteins contribute to myocardial protection, alleviating myocardial infarction. These investigations provide new information for understanding the innate cardioprotective mechanisms and developing therapeutic strategies for myocardial infarction.
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Shu Q. Liu Brandon J. Tefft (2013) conducted a review in Myocardial Infarction. Liver responses and hepatic secretory proteins (FGF21, TFF3) was evaluated on Myocardial protection. Liver responses induced by myocardial ischemia, including hepatic cell mobilization and upregulation of FGF21 and TFF3, contribute to myocardial protection and alleviate myocardial infarction.
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