Journal club of the week: The role of mitochondria in cardioprotection

Speaker: Dr Amir Hossein Abdolghaffari

Date: 25th of april, 2016

Topic: The role of mitochondria in cardioprotection

In the journal meeting on the 25th of April, 2016, Dr Amir Hossein Abdolghaffari introduced the participants to role of mitochondria in cardioprotection. He briefly talk that ischemic heart disease is the major cause of mortality and morbidity worldwide. Early reperfusion after acute myocardial ischemia has reduced short-term mortality, but it is also responsible for additional myocardial damage, which in the long run favors adverse cardiac remodeling and heart failure evolution. How mitochondrial dysfunction plays a key role in the pathogenesis of IR injury and cardiomyopathy (CM). However, despite promising mitochondria-targeted drugs emerging from the laboratory, very few have successfully completed clinical trials. As such, the mitochondrion is a potential untapped target for new IHD and CM therapies. He also talked that the main function of cardiac mitochondria is ATP synthesis via oxidative phosphorylation (Ox-Phos). After substrate oxidation, reducing equivalents generated by the tricarboxylic acid cycle are used by the respiratory chain (RC) to generate a transmembrane potential (mitochondrial membrane potential) that drives ATP synthesis. The primary pathological event in IHD is acute myocardial infarction (AMI) caused by coronary artery obstruction. Whereas permanent occlusion often results in cardiac remodeling and hypertrophy, transient occlusion is also detrimental to cardiac function, and the reperfusion phase of IR injury is particularly injurious to mitochondria. He talked about various noxious and beneficial pathways that contribute towards cardiac ischemic disease. The molecular pathways which control cell dedifferentiation/redifferentiation process in response to stress are not fully understood. However, recent research points out an important physiological role of TH signaling are responsible to cardiac activities. As clearly documented by several experimental animal data, most of the effects of TH on cardiac function are mediated by binding of biologically active T3 to nuclear TR. Thus, T3 tissue concentration represents the switching factor in TH signaling. The available evidence suggests that TH should be administered at a physiological or near-physiological dose in the early phase of the post-ischemic wound healing following reactivation of the endogenous regenerative process in order to obtain the maximal protective effect. Prof. Dr. Abdollahi put light on the whole presentation and give a brief summary. At the end all participants asked their valuable questions and he answered all the questions.