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| Author | : Shijun Wang |
| Publisher | : Frontiers Media SA |
| Total Pages | : 245 |
| Release | : 2022-07-27 |
| Genre | : Medical |
| ISBN | : 2889766209 |
| Author | : Attilio Maseri |
| Publisher | : |
| Total Pages | : 49 |
| Release | : 1995 |
| Genre | : |
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| Author | : |
| Publisher | : |
| Total Pages | : 49 |
| Release | : 1995 |
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| Author | : Attilio Maseri |
| Publisher | : |
| Total Pages | : |
| Release | : 1995 |
| Genre | : |
| ISBN | : |
| Author | : R. Ferrari |
| Publisher | : Springer Science & Business Media |
| Total Pages | : 337 |
| Release | : 2012-12-06 |
| Genre | : Medical |
| ISBN | : 146844865X |
Over the past years, the thrust of research in cardiology has been toward an understanding of the engineering of the heart as a pump that transports blood to the various organs of the body. More recently, the fields of biochemistry and biophysics have come to influence heart research. The modern cardiologist can no longer pretend to understand, for example, what is happening to the patient with myocardial infarction or ischemia without understanding the principles of molecular biology. The structure and function of the heart are therefore central themes of cardiological research and practice, which incorporate knowledge and discoveries from diverse disciplines. The importance of lipid metabolism in the myocardium has become clearly understood. In the well-oxygenated heart, fatty acids are the preferred substrates. The fact that the heart derives most of its energy from the oxidation of lipids, which represent the larg est energy store of the body, is logical for an organ that must work throughout our lifetime. There are, however, several lines of evidence that during ischemia, lipids may. be harmful to the heart. High levels of free fatty acids in the serum have been suggested to play a role in causing life-threatening arryhthmias and damage in the ischemic heart. The molecular basis for these effects remains poorly understood, and several possible mechanisms for these harm ful effects have been suggested.
| Author | : Gary D. Lopaschuk |
| Publisher | : Springer |
| Total Pages | : 301 |
| Release | : 2014-08-22 |
| Genre | : Science |
| ISBN | : 1493912275 |
The heart has a very high energy demand but very little energy reserves. In order to sustain contractile function, the heart has to continually produce a large amount of ATP. The heart utilizes free fatty acids mainly and carbohydrates to some extent as substrates for making energy and any change in this energy supply can seriously compromise cardiac function. It has emerged that alterations in cardiac energy metabolism are a major contributor to the development of a number of different forms of heart disease. It is also now known that optimizing energy metabolism in the heart is a viable and important approach to treating various forms of heart disease. Cardiac Energy Metabolism in Health and Disease describes the research advances that have been made in understanding what controls cardiac energy metabolism at molecular, transcriptional and physiological levels. It also describes how alterations in energy metabolism contribute to the development of heart dysfunction and how optimization of energy metabolism can be used to treat heart disease. The topics covered include a discussion of the effects of myocardial ischemia, diabetes, obesity, hypertrophy, heart failure, and genetic disorders of mitochondrial oxidative metabolism on cardiac energetics. The treatment of heart disease by optimizing energy metabolism is also discussed, which includes increasing overall energy production as well as increasing the efficiency of energy production and switching energy substrate preference of the heart. This book will be a valuable source of information to graduate students, postdoctoral fellows, and investigators in the field of experimental cardiology as well as biochemists, physiologists, pharmacologists, cardiologists, cardiovascular surgeons and other health professionals.
| Author | : Jimmy Zhang |
| Publisher | : |
| Total Pages | : 171 |
| Release | : 2018 |
| Genre | : |
| ISBN | : |
Ischemia-reperfusion (IR) injury is the underlying pathology of acute myocardial infarction. The severity of IR injury is driven by mitochondrial metabolism and modulated by mitochondrial quality control mechanisms. The Krebs' cycle metabolite succinate is central to IR injury. Succinate accumulates during ischemia and its oxidation at reperfusion drives injury. The mechanism of ischemic succinate accumulation is controversial, and is proposed to involve reversal of mitochondrial complex-II. Here, using stable isotope resolved metabolomics, we demonstrated that complex-II reversal was possible in hypoxic mitochondria, but was not the primary source of succinate in hypoxic cardiomyocytes or ischemic hearts. Rather, in these intact systems succinate primarily originated from canonical Krebs' cycle activity, partly supported by aminotransferase anaplerosis and glycolysis from glycogen. Augmentation of canonical Krebs' cycle activity with dimethyl-?-ketoglutarate both increased ischemic succinate accumulation and drove substrate-level phosphorylation by succinyl-CoA synthetase, improving ischemic energetics. Although ? of ischemic succinate accumulation was extracellular, the remaining ? was metabolized during early reperfusion, wherein acute complex-II inhibition was protective. These results highlight a bifunctional role for succinate: its complex-II independent accumulation being beneficial in ischemia, and its complex-II dependent oxidation being detrimental at reperfusion. IR injury is also modulated by mitochondrial quality control mechanisms, such as autophagy. Mild mitochondrial uncoupling induces mitochondrial autophagy and both have separately been shown to protect against cardiac IR injury. However, a link between mild uncoupling and autophagy within the context of cardiac IR injury or cardioprotection has not been explored experimentally or therapeutically. Previously, we identified cloxyquin via phenotypic screening as a cardioprotective compound. Here, we demonstrated that cloxyquin mildly uncoupled mitochondria and induced autophagy. Cloxyquin-induced cardioprotection was blocked by the autophagy inhibitor chloroquine. Finally, we showed that cloxyquin-induced cardioprotection translated to an in vivo model of cardiac IR injury. Overall, these data suggest that enhanced insights into the molecular events that take place at mitochondria during ischemia may be exploited for therapeutic benefit in cardiac IR injury.
| Author | : Pierce A. Grace |
| Publisher | : Wiley-Blackwell |
| Total Pages | : 400 |
| Release | : 1999-02-04 |
| Genre | : Medical |
| ISBN | : 9780632050215 |
Ischaemia-Reperfusion Injury is concerned with the consequences of interrupting and restoring blood flow to tissues. Many common clinical conditions are caused by interruption of blood flow to tissues (eg, ischaemic heart disease, peripheral vascular disease, stroke); blood flow is also interrupted deliberately in many surgical procedures (eg, cardiac surgery, arterial surgery, transplant surgery, limb surgery with tourniquet). In treating such conditions or after performing such operations the aim of the clinician is to restore the blood supply to the ischaemic tissue. Paradoxically, restoration of blood flow to ischaemic tissues can lead to further tissue damage with the potential for severe local and systemic injury. This book focuses on the clinical, pathological and biochemical processes involved in ischaemia-reperfusion injury and gives an overview of the strategies that may be adopted to mitigate or prevent such injury. This book will be of interest to both clinicians and scientists who have to deal with or have interest in this difficult but important problem.
| Author | : Gaetano Santulli |
| Publisher | : Springer |
| Total Pages | : 644 |
| Release | : 2017-05-25 |
| Genre | : Science |
| ISBN | : 3319553305 |
This text covers the basic principles of mitochondrial dynamics in cardiovascular medicine, with particular emphasis on their functional roles in physiology and disease. The book will include articles pertaining to mitochondrial fitness on a global basis, providing therefore an update on the progress made in several aspects in the field. Thus, it will assist scientists and clinicians alike in furthering basic and translational research. Organized in sections focusing on: basic science, mitochondrial dysfunction in cardiac disorders, in vascular disorders, in metabolic disorders, in kidney disease, therapeutic challenges and options, this essential volume fills imperative gaps in understanding and potentially treating several cardiovascular disorders.
| Author | : José Marín-García |
| Publisher | : Springer Science & Business Media |
| Total Pages | : 415 |
| Release | : 2005-05-05 |
| Genre | : Medical |
| ISBN | : 0387255745 |
Mitochondria have been pivotal in the development of some of the most important ideas in modern biology. Since the discovery that the organelle has its own DNA and specific mutations were found in association with neuromuscular and cardiovascular diseases and with aging, an extraordi-nary number of publications have followed, and the term mitochondrial medicine was coined. Furthermore, our understanding of the multiple roles that mitochondria play in cardiac cell homeostasis opened the door for intensive experimentation to understand the pathogenesis and to find new treatments for cardiovascular diseases. Besides its role in adenosine triphosphate generation, mitochondria regu-late a complex network of cellular interactions, involving (1) generation and detoxification of reactive oxygen species, including superoxide anion, hy-drogen peroxide, and hydroxyl radical; (2) maintenance of the antioxidant glutathione in a reduced state and adequate level of mitochondrial matrix superoxide dismutase; (3) cytoplasmic calcium homeostasis, particularly under conditions of cellular calcium loading; (4) transport of metabolites between cytoplasm and matrix; (5) both programmed (apoptosis) and necrotic cell death; and (6) cell growth and development. It is therefore not surprising that this organelle has come to be the center stage in many current investigations of cardiovascular diseases, aging, and agi- related disease. Concomitant with these advances, an impressive effort is under- way for the development of new tools and methodologies to study mitochondrial structure and function, including powerful ways to visualize, monitor, and alter the organelle function to assess the genetic consequences of these perturbations.
