Journal
CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY
Volume 95, Issue 10, Pages 1163-1169Publisher
CANADIAN SCIENCE PUBLISHING
DOI: 10.1139/cjpp-2016-0609
Keywords
myocardial ischemia; ischemic preconditioning; heart failure; cell death; necroptosis; passive necrosis
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Funding
- Slovak Scientific Grant Agency (VEGA) [VEGA 1/0271/16, 2/0201/15, APVV-15-607, APVV-0102-11]
- Slovak Society of Cardiology
- Ministry of Health of the Czech Republic [15-27735A]
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Long-lasting ischemia can result in cell loss; however, repeated episodes of brief ischemia increase the resistance of the heart against deleterious effects of subsequent prolonged ischemic insult and promote cell survival. Traditionally, it is believed that the supply of blood to the ischemic heart is associated with release of cytokines, activation of inflammatory response, and induction of necrotic cell death. In the past few years, this paradigm of passive necrosis as an uncontrolled cell death has been re-examined and the existence of a strictly regulated form of necrotic cell death, necroptosis, has been documented. This controlled cell death modality, resembling all morphological features of necrosis, has been investigated in different types of ischemia-associated heart injuries. The process of necroptosis has been found to be dependent on the activation of RIP1-RIP3-MLKL axis, which induces changes leading to the rupture of cell membrane. This pathway is activated by TNF-alpha, which has also been implicated in the cardioprotective signaling pathway of ischemic preconditioning. Thus, this review is intended to describe the TNF-alpha-mediated signaling leading to either cell survival or necroptotic cell death. In addition, some experimental data suggesting a link between heart dysfunction and the cellular loss due to necroptosis are discussed in various conditions of myocardial ischemia.
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