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Mitochondria: the cell powerhouse and nexus of stress

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889192830 Year: Pages: 121 DOI: 10.3389/978-2-88919-283-0 Language: English
Publisher: Frontiers Media SA
Subject: Biology --- Physiology --- Science (General)
Added to DOAB on : 2015-12-10 11:59:06
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Mitochondrion, a sub-cellular organelle originated from primary endosymbiosis, plays a vital role in energy metabolism of eukaryotic cells. The transfer of electrons through the electron transport chain (ETC) to molecular oxygen accompanied by the extrusion of protons from the matrix generate an electrochemical gradient across the inner mitochondrial membrane (IMM) that is used for ATP synthesis by oxidative phosphorylation. Despite many aspects of ATP synthesis have been delineated, regulatory mechanisms responsible for energy synthesis and transfer still remain to be uncovered. In addition to energy function, mitochondria play a crucial role in cell metabolism under both physiological and pathological conditions through their participation in many intracellular signaling pathways. Studies over the last 30 years provide strong evidence that mitochondria are the nexus of various stresses which initiate cell death through apoptosis, oncosis, necrosis and autophagy depending on the severity of the stress and cellular energy status. The release of several pro-apoptotic proteins such as cytochrome c, Smac/DIABLO, AIF, endonuclease G from intermembrane space initiates both caspase-dependent and caspase-independent apoptosis. The formation of the mitochondrial permeability transition pore in the IMM promotes cell death mostly through necrosis whereas a mild stress activates autophagy. Due to their critical roles in both cell death and survival mitochondria have been widely considered as an important target for various pharmacological and conditional therapeutic approaches. Currently, a large number of mitochondria-targeted agents are suggested to prevent (in ischemia reperfusion injury, cardiovascular, neurodegenerative and other diseases) or stimulate (in various cancers) cell death. This Research Topic focuses on the role of mitochondria in the regulation of cell metabolism and signaling under physiological and pathological conditions. Studies performed on cultured cells and isolated organs/tissues using different animal and cellular models of various diseases are also included and discussed.

Restricted Growth - Clinical, Genetic and Molecular Aspects

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ISBN: 9789535126942 9789535126959 Year: Pages: 174 DOI: 10.5772/61620 Language: English
Publisher: IntechOpen
Subject: Genetics
Added to DOAB on : 2019-10-03 07:51:49

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Restricted growth conditions are a group of genetic disorders with primary effect on growth (short stature); it is very heterogeneous and comprises two important categories: skeletal dysplasia and different genetic syndromes with primary effect on growth. It could also be caused by a medical condition. The book contains chapters regarding different aspects of the study of restricted growth that are divided into three broad sections. Section I: Defining Restricted Growth, Section II: Genetics and Diagnosis of Restricted Growth, and Section III: Signaling Pathways and Molecular Mechanisms of Restricted Growth. The book presents comprehensive reviews of each topic written by experts in the field. It will be the most valuable tool for physicians and life science researchers and students. We hope that the book will motivate discussion and research in this important health problem, setting the path for better therapeutic approaches.

Mitochondrial Diseases

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ISBN: 9781789236743 9781789236750 Year: Pages: 496 DOI: 10.5772/67963 Language: English
Publisher: IntechOpen
Subject: Genetics
Added to DOAB on : 2019-10-03 07:51:51

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Mitochondria are crucial organelles for any cell type. Mitochondria take responsibility for not only energy production but also regulation of cell death, also called apoptosis; calcium storage; and heat production. Therefore, mitochondrial disease is implicated in the mode of action of many harmful factors for cells such as drugs and environmental contaminants, dysfunction of the oxygen transport system, malnutrition, intense exercise, and genetic variations. This book presents up-to-date knowledge about mitochondrial disease and its complex relation to some diseases such as cardiac failure, cancer, and Alzheimer's and Parkinson's diseases. This book will, therefore, be essential for readers who are interested in life sciences, especially in medicine.

Mitochondrial DNA - New Insights

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ISBN: 9781789842654 9781789842661 Year: Pages: 224 DOI: 10.5772/intechopen.72029 Language: English
Publisher: IntechOpen
Subject: Genetics
Added to DOAB on : 2019-10-03 07:51:52

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The very short genomes of mitochondria summarize the complexity of molecular biology and its interactions with cellular and whole organism biology. Studies of mitogenomes contribute to the understanding of molecular biology and evolution, and to health management. Despite or even due to their small sizes, mitogenomes continue to surprise us. Studies of mitogenomes reveal the details of molecular organization and its evolution under constraints for miniaturization.

Current Strategies for the Biochemical Diagnosis and Monitoring of Mitochondrial Disease

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ISBN: 9783038972402 9783038972419 Year: Pages: 238 DOI: 10.3390/books978-3-03897-241-9 Language: English
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Medicine (General) --- Public Health --- Therapeutics
Added to DOAB on : 2018-10-16 10:00:26
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Mitochondrial disease constitutes a complex and heterogeneous group of disorders resulting from a defect in mitochondrial respiratory chain (MRC) enzyme activity. In view of the dual regulation of the MRC, exercised by both the mitochondrial and nuclear genome, mutations in either mitochondrial or nuclear DNA can result in a MRC deficiency. Whilst a single organ can be affected, MRC disorders often result in a multi-organ system presentation with prominent neurological and myopathic features. The diagnosis of MRC disorders can be complex, and requires a coordinated interplay of a number of disciplines. However, biochemical determination of metabolites in blood, cerebral spinal fluid (CSF) and/or urine are generally considered to be first-line investigations for the diagnosis of these disorders, although they lack sensitivity and specificity. Furthermore, there is a lack of consensus on the overall utility of monitoring other biochemical parameters, which may be of diagnostic value. For example, although oxidative stress may contribute to the pathogenesis of mitochondrial disorders, few centers monitor this as part of their diagnostic repertoire. Therefore, the purpose of this Special Issue was to highlight potential biomarkers of mitochondrial disease and to discuss the appropriateness of biochemical markers to monitor disease progression and therapeutic intervention.

Mitochondrial Dysfunction in Ageing and Diseases

ISBN: 9783038422518 9783038422525 Year: Pages: XXVI, 516 Language: English
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Added to DOAB on : 2016-08-16 07:37:51
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The past decade has witnessed an explosion of knowledge regarding how mitochondrial dysfunction may translate into ageing and disease phenotypes, as well as how it is modulated by genetic and lifestyle factors. Impairment of the mitochondria may be caused by mutations or deletions in nuclear or mitochondrial DNA. Hallmarks of mitochondrial dysfunction include decreased ATP production, decreased mitochondrial membrane potential, swollen mitochondria, damaged cristae, increased oxidative stress, and decreased mitochondrial DNA copy number. In addition to energy production, mitochondria play an important role in regulating apoptosis, buffering calcium release, retrograde signaling to the nuclear genome, producing reactive oxygen species (ROS), participating in steroid synthesis, signaling to the immune system, as well as controlling the cell cycle and cell growth. Dysfunctional mitochondria have been implicated in ageing and in several diseases, many of which are age-related, including mitochondrial diseases, cancers, metabolic diseases and diabetes, inflammatory conditions, neuropathy, and neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and Huntington’s disease. Additionally, a possible link between mitochondrial metabolism and the ubiquitin-proteasome and autophagy-lysosome systems is emerging as a novel factor contributing to the progression of several human diseases. This special issue calls for original research, mini and full reviews, and perspectives that address the progress and current standing in the vast field of mitochondrial biology. These include, but are not limited to: ageingneurodegenerative diseasesmitochondrial diseasesmetabolic diseasesprotein homeostasiscell/retrograde signalingoxidative stresspaincancerimmune systemtherapies to counteract mitochondrial dysfunction

Mitochondria in Skeletal Muscle Health, Aging and Diseases

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889450732 Year: Pages: 142 DOI: 10.3389/978-2-88945-073-2 Language: English
Publisher: Frontiers Media SA
Subject: Physiology --- Science (General)
Added to DOAB on : 2017-07-06 13:27:36
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Skeletal muscle is the most abudant tissue of the human body, making up to 40 to 50% of the human body mass. While the importance of optimal muscle function is well recognized in the athletic field, its significance for general health is often underappreciated. In fact, the evidence that muscle mass, strength and metabolism are essential for our overall health is overwhelming. As the largest protein reservoir in the human body, muscles are essential in the acute response to critical illness such as sepsis, advanced cancer, and traumatic injury. Loss of skeletal muscle mass has also been associated with weakness, fatigue, insulin resistance, falls, fractures, frailty, disability, several chronic diseases and death. As a consequence, maintaining skeletal muscle mass, strength and metabolism throughout the lifespan is critical to the maintenance of whole body health. Mitochondria are fascinating organelles regulating many critical cellular processes for skeletal muscle physiology, including for instance energy supply, reactive oxygen species production, calcium homeostasis and the regulation of apoptosis. It is therefore not surprising that mitochondrial dysfunction has been implicated in a large number of adverse events/conditions and pathologies affecting skeletal muscle health. While the importance of normal mitochondrial function is well recognized for muscle physiology, there are important aspects of mitochondrial biology that are still poorly understood. These include mitochondrial dynamics (fusion and fission processes), morphology and processes involved in mitochondrial quality control (mitophagy). Defining the mechanisms regulating these different aspects of mitochondrial biology, their importance for muscle physiology, as well as the interrelations will be critical for expanding understanding of the role played by mitochondria in skeletal muscle physiology and health. The present research topic provides readers with novel experimental approaches, knowledge, hypotheses and findings related to all aspects of mitochondrial biology in healthy and diseased muscle cells.Skeletal muscle is the most abudant tissue of the human body, making up to 40 to 50% of the human body mass. While the importance of optimal muscle function is well recognized in the athletic field, its significance for general health is often underappreciated. In fact, the evidence that muscle mass, strength and metabolism are essential for our overall health is overwhelming. As the largest protein reservoir in the human body, muscles are essential in the acute response to critical illness such as sepsis, advanced cancer, and traumatic injury. Loss of skeletal muscle mass has also been associated with weakness, fatigue, insulin resistance, falls, fractures, frailty, disability, several chronic diseases and death. As a consequence, maintaining skeletal muscle mass, strength and metabolism throughout the lifespan is critical to the maintenance of whole body health. Mitochondria are fascinating organelles regulating many critical cellular processes for skeletal muscle physiology, including for instance energy supply, reactive oxygen species production, calcium homeostasis and the regulation of apoptosis. It is therefore not surprising that mitochondrial dysfunction has been implicated in a large number of adverse events/conditions and pathologies affecting skeletal muscle health. While the importance of normal mitochondrial function is well recognized for muscle physiology, there are important aspects of mitochondrial biology that are still poorly understood. These include mitochondrial dynamics (fusion and fission processes), morphology and processes involved in mitochondrial quality control (mitophagy). Defining the mechanisms regulating these different aspects of mitochondrial biology, their importance for muscle physiology, as well as the interrelations will be critical for expanding understanding of the role played by mitochondria in skeletal muscle physiology and health. The present research topic provides readers with novel experimental approaches, knowledge, hypotheses and findings related to all aspects of mitochondrial biology in healthy and diseased muscle cells.

Pathophysiological Mechanisms of Sarcopenia in Aging and in Muscular Dystrophy: A Translational Approach

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889196845 Year: Pages: 248 DOI: 10.3389/978-2-88919-684-5 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2016-04-07 11:22:02
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Loss of muscle mass and increased fibrosis characterize both sarcopenia of aging and muscular dystrophy. Research is increasingly showing that these two conditions also share several pathophysiological mechanisms, including mitochondrial dysfunction, increased apoptosis, abnormal modulation of autophagy, decline in satellite cells, increased generation of reactive oxygen species, and abnormal regulation of signaling and stress response pathways. This Research Topic will cover several mechanisms involved in aging and dystrophic sarcopenia and explore the therapeutic potential of various strategies for intervention.

Hypoxia in Kidney Disease

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889456178 Year: Pages: 143 DOI: 10.3389/978-2-88945-617-8 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Physiology
Added to DOAB on : 2019-01-23 14:53:43
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Kidney disease is a complex health problem, often coinciding with cardiovascular pathology (e.g. hypertension) and metabolic disturbances (e.g. obesity and diabetes). It is also a disturbingly fast growing global public health problem, e.g. chronic kidney disease affects an estimated ~9-16% of the population. Besides the public health issues this results in a large economic burden as kidney diseases contributes disproportionally to about a quarter of total health care costs. Experimental and clinical data solidly support the view that kidney tissue hypoxia plays a critical and intricate role during the genesis and progression of both chronic and acute kidney diseases. This research field is currently at the very beginning of integrating pre-clinical with clinical research in which hypoxia related mechanism are quantified by non-invasive imaging. In combination with the fact that some key questions remain unanswered, this offers exciting new research perspectives that are waiting to be explored. With this Research Topic we aim to discuss and find answers to the following research question: 1) What are the temporal relationships between hypoxia and kidney disease? 2) Can we demonstration causation between hypoxia and kidney disease? 3) Can renal hypoxia be considered as a treatment target in kidney disease? 4) Can hypoxia (e.g. in the urine) be considered a biomarker of kidney disease? 5) Does hypoxia ramp-up sympathetic activity? 6) Does hypoxia trigger inflammation? 7) Is hypoxia caused by changes in sodium reabsorption and/or mitochondrial function? 8) Which molecular mechanisms are involved in hypoxia in kidney disease? 9) Which gene expressions change due to hypoxia in kidney disease? 10) Can we generate new and translational insights using non-invasive imaging technologies? Our overall aim is identify the mediators/controllers of hypoxia in kidney disease. If we understand more about the sequence of events leading to hypoxia, its regulation and consequences in renal disease, we might be able to have a major impact in clinical practice. I.e. more accurate and earlier diagnosis, novel treatment targets, and novel therapies.

Mitochondrial Dysfunction in Aging and Diseases of Aging

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ISBN: 9783039213276 9783039213283 Year: Pages: 270 DOI: 10.3390/books978-3-03921-328-3 Language: English
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Science (General) --- Biology
Added to DOAB on : 2019-12-09 11:49:15
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This collection of review articles authored by international experts pulls together current information about the role of mitochondria in aging and diseases of aging. Mitochondria are vitally important cellular organelles and undergo their own aging process becoming less efficient in aged animals including humans. These changes have wide-ranging significance contributing to immune dysfunction (autoimmunity and immune deficiency), inflammation, delayed healing, skin and retinal damage, cancer and most of the degenerative diseases of aging. Mitochondrial aging predisposes to drug toxicity in the geriatric population and to many of the features of normal aging. The research detailed in this book summarizes current understanding of the role of mitochondria in the complex molecular changes of aging, moving on to specific diseases of aging. Mitochondrial dysfunction is an important target for development of treatments for aging and disease. The last article details how exercise is a treatment and combats many features of the aging process.

Keywords

aging --- mitochondria --- inflammation --- innate immunity --- adaptive immunity --- immunosenescence --- cell danger response --- healing cycle --- mitochondria --- purinergic signaling --- metabokines --- sphingolipids --- integrated cell stress response --- de-emergence --- crabtree effect --- pasteur effect --- coenzyme Q10 --- aging --- age-related diseases --- mitochondrial dysfunction --- mitochondria --- skin --- ageing --- reactive oxygen species --- photoageing --- 25(OH)D --- 1,25(OH)2D --- aging --- cytokines --- inflammation --- morbidity and mortality --- prevention --- reactive oxygen species --- ultraviolet --- aging --- mitochondria --- retina --- optic nerve --- diabetic retinopathy --- age-related macular degeneration --- glaucoma --- drug-induced mitochondrial toxicity --- polypharmacy --- aging --- mitochondrial dysfunction --- insulin resistance --- type 2 diabetes --- mitochondrial transfer --- exosomes --- mitochondrial --- genetic mutations --- cardiovascular disease --- heart failure --- cardiomyopathy --- mitochondria --- cancer --- nucleotide metabolism --- DNA damage --- NAD+ --- mitochondria --- ALS --- axonal transport --- mitophagy --- SOD1 --- Miro1 --- PINK1 --- Parkin --- multiple sclerosis --- mitochondria --- neuroinflammation --- neurodegeneration --- Parkinson’s disease --- mitochondria --- ageing --- neurodegenerative disease --- Alzheimer’s disease --- eIF2? --- metabolism --- mitochondria --- proteostasis --- stress response --- aging --- exercise --- mitochondria --- aerobic --- ROS --- inflammation --- senescence --- lysosome --- autophagy --- mitophagy --- n/a

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