Mitochondrial Involvement in the Molecular Mechanisms of Ischemia-Reperfusion Injury in the Heart | Chapter 6 | Recent Research Advances in Biology Vol. 8

 Mitochondria are responsible for maintaining cell viability and essential biological activities by producing energy (ATP). These organelles are also a major source of reactive oxygen species (ROS) and a number of apoptosis inducers. The importance of mitochondria in a variety of areas of cell physiology and pathology, such as intracellular signaling, has been demonstrated. Mitochondria and mitochondrial function can decline as a result of pathological situations such as illness, ischemia-reperfusion injury, and ageing. Due to numerous cell stressors, creation of excess ROS (oxidative stress), elevated cellular and mitochondrial calcium levels, and apoptotic or necrotic cell death, damaged or injured mitochondria are the main causes of cell and tissue abnormalities. Under normal and pathological settings, the relationship between these mitochondrial activities has yet to be identified. Mitochondria are intimately implicated in a variety of pathophysiological pathways in cardiac IR injury. The role of mitochondrial dynamics (fission, fusion) and heterogeneity is discussed here. We emphasise the existence of functionally distinct mitochondrial subpopulations in the heart and skeletal muscles, which may have varied susceptibility to illnesses and IR injury. As a result, various cardioprotective medications that maintain mitochondrial stability, dynamics, and turnover, such as several agents, specific mitochondrial antioxidants, uncouplers, and the use of ischemic preconditioning, may be considered as possible, beneficial strategies to protect mitochondria and cardiac function and extend lifespan.

Author (s) Details

Andrey V. Kuznetsov
Cardiac Surgery Research Laboratory, Department of Cardiac Surgery, Innsbruck Medical University, 6020 Innsbruck, Austria and Department of Paediatrics I, Medical University of Innsbruck, 6020 Innsbruck, Austria.

Sabzali Javadov
Department of Physiology, School of Medicine, University of Puerto Rico, San Juan, PR 00936-5067, USA.

Michael J. Ausserlechner
Department of Paediatrics I, Medical University of Innsbruck, 6020 Innsbruck, Austria.

Judith Hagenbuchner
Department of Paediatrics II, Medical University of Innsbruck, 6020 Innsbruck, Austria.

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Liver Transplantation Studies Using a Canine Model: A Zoom on the Intermediate Filaments of the Cytoskeleton of the Hepatocytes | Chapter 3 | Highlights on Medicine and Medical Research Vol. 9

 Liver transplantation can be used to treat both acute and chronic liver insufficiency. Graft malfunction persists in the twenty-first century. It affects up to one-third of those who receive it, despite reports of good to exceptional long-term outcomes. The etiologic examination of organ dysfunction revealed a complex basis at the time of authoring this chapter. Ischemia and reperfusion (I/R) injury is arguably the most major contributing factor for organ dysfunction, despite the numerous etiology. Cholestasis, or the cessation or reduction of bile flow with or without bile, is a condition in which the flow of bile is stopped or reduced. I/R damage is frequently accompanied with duct loss or ductopenia, as well as biliary ductular proliferations. They can, however, be deceiving, as they can also be present in other types of graft malfunction. Biliary marker levels often rise within 5 days of donation. The intermediate filaments of the cytoskeleton were studied in detail in this chapter using a liver transplantation model as an I/R damage model. The phenotypic flip of hepatocytes occurs before frank cholestasis, according to our findings. We believe that focusing on this phenotypic transformation in liver cells could aid in the savage or improved fate of the liver transplantation.

Author (s) Details

Consolato M. Sergi
Department of Laboratory Medicine and Pathology, University of Alberta, Edmonton, AB, Canada and Stollery Children’s Hospital, University Alberta Hospital, Edmonton, AB, Canada.

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