The Role of Mitochondria in Cardio-Immunology in Response to Stress Heart Conditions

Dear Colleagues,

Approximately 1.5 million adults in the U.S. have had a Myocardial Infraction (MI). Today, treatment for an MI can ameliorate one’s lifestyle, but there is lasting substantial necrosis to the heart muscle and cardiomyocytes. Around 30% of the human heart is constituted by cardiomyocytes, whereas the other 70% is made up of cardiac fibroblasts, endothelial cells, stem cells and macrophages.

Macrophages appear to be essential following an MI. In particular, healing begins when the inflammatory signals recruit macrophages and monocytes to the site of the damage. First, the macrophages remove the damaged tissue, secreting proteolytic enzymes through inflammatory stimuli. The next phase is characterized by the ingestion/differentiation of myofibroblasts and recruitment from the expression of a-SMA (alpha smooth muscle actin) from the deposition of collagen and angiogenesis “heart-failure remodeling”. Macrophages additionally provide support to the immune system, and they also control transcriptional and post-transcriptional events after a Myocardial Infarction. Pro-inflammatory M1 macrophages display decreased oxygen consumption levels and an enhanced rate of glycolysis during phagocytosis or upon activation by an inflammatory stimulus. Indeed, the pro-inflammatory macrophages utilize glycolysis and the pentose phosphate pathway (PPP) to meet the ATP requirements. Pro-inflammatory macrophages can also control the Krebs cycle at two points, downregulating OXPHOS and fatty acid oxidation (FAO). In M2 anti-inflammatory macrophages, the Krebs cycle is intact, and their metabolic activity is characterized by enhanced FAO and OXPHOS. Based on these data, the mitochondria in macrophages play an essential role in response to an MI, in a process called “immune-metabolism”. During both the processes, macrophage polarization and turnover involve metabolic reprogramming, and thus mitochondrial “immune-metabolism”. Macrophages, in addition to supporting immune activity in specific contexts, need metabolic adaptations that directly affect the immune cell functions by controlling the transcriptional and post-transcriptional events. Moreover, some recent studies have shown that mitochondrial MFN2 is a master regulator of these immune responses. MFN2 is highly expressed in macrophages particularly upon the application of immune stress such as by pro-inflammatory activators.

The goal of this issue is to highlight the recent advances related to the mitochondrial metabolism mediated by Mfn2 in cardiac macrophages in response to an MI for future therapeutic approaches in vivo.

Dr. Antonietta Franco
Dr. Xiawei Dang
Guest Editors

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• mitochondria metabolism
• myocardial infraction
• cardiac repair
• immune cardiac metabolism
• mitochondria macrophages