Medical College of Wisconsin
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Cardioprotective mechanisms activated in response to myocardial ischemia. Mol Cell Biomech 2011 Dec;8(4):319-38

Date

02/18/2012

Pubmed ID

22338709

Scopus ID

2-s2.0-84555190225 (requires institutional sign-in at Scopus site)   31 Citations

Abstract

Myocardial ischemia, a disorder causing myocardial infarction and malfunction, can activate various adaptive mechanisms that protect cardiomyocytes from ischemic injury. During the early hours post myocardial ischemia, injured cardiac cells can release several molecules, including adenosine, opioids, and bradykinin, which promote myocardial survival by activating the G protein signaling pathways. During a later phase about several days, myocardial ischemia induces upregulation of growth factors and cytokines, including VEGF, ILGF, HGF, and SDF-1, in the injured myocardium, contributing to cardioprotection. In addition to the injured heart, the liver participates in cardioprotection. In response to myocardial ischemia, the liver upregulates and releases secretory proteins, including FGF21 and TFF3, both of which promote cardiomyocyte survival. The liver also provides a reservoir of hepatic cells that mobilize to the site of myocardial ischemia, potentially contributing to cardioprotection. Taken together, the early and late mechanisms act coordinately in a time-dependent manner, ensuring effective cardioprotection post myocardial infarction. Investigations on these innate cardioprotective mechanisms have provided insights into the development of cardioprotective strategies for treating myocardial infarction. In this article, the authors review the innate mechanisms of cardioprotection in myocardial ischemia.

Author List

Liu SQ, Tefft BJ, Zhang D, Roberts D, Schuster DJ, Wu A

Author

Brandon J. Tefft PhD Associate Professor in the Biomedical Engineering department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Cytokines
Cytoprotection
Humans
Intercellular Signaling Peptides and Proteins
Liver
Myocardial Ischemia
Myocardium
Myocytes, Cardiac
Signal Transduction