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Ethylene: A Key Regulatory Molecule in Plants

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889453412 Year: Pages: 310 DOI: 10.3389/978-2-88945-341-2 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Botany --- Physiology
Added to DOAB on : 2018-11-22 11:28:10
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Ethylene is a simple gaseous phytohormone with multiple roles in regulation of metabolism at cellular, molecular, and whole plant level. It influences performance of plants under optimal and stressful environments by interacting with other signaling molecules. Understanding the ethylene biosynthesis and action through the plant’s life can contribute to improve the knowledge of plant functionality and use of this plant hormone may drive adaptation and defense of plants from the adverse environmental conditions. The action of ethylene depends on its concentration in cell and the sensitivity of plants to the hormone. In recent years, research on ethylene has been focused, due to its dual action, on the regulation of plant processes at physiological and molecular level. The involvement of ethylene in the regulation of transcription needs to be widely explored involving the interaction with other key molecular regulators. The aim of the current research topic was to explore and update our understanding on its regulatory role in plant developmental mechanisms at cellular or whole plant level under optimal and changing environmental conditions. The present edited volume includes original research papers and review articles describing ethylene’s regulatory role in plant development during plant ontogeny and also explains how it interacts with biotic and abiotic stress factors. This comprehensive collection of researches provide evidence that ethylene is essential in different physiological processes and does not always work alone, but in coordinated manner with other plant hormones. This research topic is also a source of tips for further works that should be addressed for the biology and molecular effects on plants.

Molecular Mechanisms and Physiological Significance of Organelle Interactions and Cooperation

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889451043 Year: Pages: 151 DOI: 10.3389/978-2-88945-104-3 Language: English
Publisher: Frontiers Media SA
Subject: Biology --- Science (General)
Added to DOAB on : 2017-07-06 13:27:36
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Eukaryotic cells contain distinct membrane-bound organelles, which compartmentalise cellular proteins to fulfil a variety of vital functions. Many organelles have long been regarded as isolated and static entities (e.g., peroxisomes, mitochondria, lipid droplets), but it is now evident that they display dynamic changes, interact with each other, share certain proteins and show metabolic cooperation and cross-talk. Despite great advances in the identification and characterisation of essential components and molecular mechanisms associated with the biogenesis and function of organelles, information on how organelles interact and are incorporated into metabolic pathways and signaling networks is just beginning to emerge. Organelle cooperation requires sophisticated targeting systems which regulate the proper distribution of shared proteins to more than one organelle. Organelle motility and membrane remodeling support organelle interaction and contact. This contact can be mediated by membrane proteins residing on different organelles which can serve as molecular tethers to physically link different organelles together. They can also contribute to the exchange of metabolites and ions, or act in the assembly of signaling platforms. In this regard organelle communication events have been associated with important cellular functions such as apoptosis, antiviral defense, organelle division/biogenesis, ROS metabolism and signaling, and various metabolic pathways such as breakdown of fatty acids or cholesterol biosynthesis. In this research topic we will focus on recent novel findings on the underlying molecular mechanisms and physiological significance of organelle interaction and cooperation with a particular focus on mitochondria, peroxisomes, endoplasmic reticulum, lysosomes and lipid droplets and their impact on the regulation of cellular homeostasis. Our understanding of how organelles physically interact and use cellular signaling systems to coordinate functional networks between each other is still in its infancy. Nevertheless recent discoveries of defined membrane structures such as the mitochondria-ER associated membranes (MAM) are revealing how membrane domains enriched in specific proteins transmit signals across organelle boundaries, allowing one organelle to influence the function of another. In addition to its role as a mediator between mitochondria and the ER, contacts between the MAM and peroxisomes contribute to antiviral signaling, and specialised regions of the ER are supposed to initiate peroxisome biogenesis, whereas intimate contacts between peroxisomes, lipid droplets and the ER mediate lipid metabolism. In line with these observations it is tempting to speculate that further physical contact sites between other organelles exist. Alternatively, novel regulated vesicle trafficking pathways between organelles (e.g., mitochondria to peroxisomes or lysosomes) have been discovered implying another mode of organelle communication. Identifying the key molecular players of such specialised membrane structures will be a prerequisite to understand how organelle communication is physically accomplished and will lead to the identification of new regulatory networks. In addition to the direct transmission of interorganellar information, cytosolic messenger systems (e.g., kinase/phosphatase systems or redox signaling) may contribute to the coordination of organelle functions. This research topic will integrate new findings from both modes of communication and will provide new perspectives for the functional significance of cross-talk among organelles. We would like to thank all the researchers who contributed their valuable work to this research topic. Furthermore, we are grateful to the reviewers and Associate Editors who contributed valuable comments and positive criticism to improve the contributions.

ACTH Action in the Adrenal Cortex: From Molecular Biology to Pathophysiology

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889452323 Year: Pages: 421 DOI: 10.3389/978-2-88945-232-3 Language: English
Publisher: Frontiers Media SA
Subject: Internal medicine --- Medicine (General)
Added to DOAB on : 2017-10-13 14:57:01
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By stimulating adrenal gland and corticosteroid synthesis, the adrenocorticotropic hormone (ACTH) plays a central role in response to stress. In this Research Topic, a particular attention has been given to the recent developments on adrenocortical zonation; the growth-promoting activities of ACTH; the various steps involved in acute and chronic regulation of steroid secretion by ACTH, including the effect of ACTH on circadian rhythms of glucocorticoid secretion. The Research Topic also reviews progress and challenges surrounding the properties of ACTH binding to the MC2 receptor (MC2R), including the importance of melanocortin-2 receptor accessory protein (MRAP) in MC2R expression and function, the various intracellular signaling cascades, which involve not only protein kinase A, the key mediator of ACTH action, but also phosphatases, phosphodiesterases, ion channels and the cytoskeleton. The importance of the proteins involved in the cell detoxification is also considered, in particular the effect that ACTH has on protection against reactive oxygen species generated during steroidogenesis. The impact of the cellular microenvironment, including local production of ACTH is discussed, both as an important factor in the maintenance of homeostasis, but also in pathological situations, such as severe inflammation. Finally, the Research Topic reviews the role that the pituitary-adrenal axis may have in the development of metabolic disorders. In addition to mutations or alterations of expression of genes encoding components of the steroidogenesis and signaling pathways, chronic stress and sleep disturbance are both associated with hyperactivity of the adrenal gland. A resulting effect is increased glucocorticoid secretion inducing food intake and weight gain, which, in turn, leads to insulin and leptin resistance. These aspects are described in detail in this Research Topic by key investigators in the field. Many of the aspects addressed in this Research Topic still represent a stimulus for future studies, their outcome aimed at providing evidence of the central position occupied by the adrenal cortex in many metabolic functions when its homeostasis is disrupted. An in-depth investigation of the mechanisms underlying these pathways will be invaluable in developing new therapeutic tools and strategies.

Plants; Stress & Proteins

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889452675 Year: Pages: 323 DOI: 10.3389/978-2-88945-267-5 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Botany
Added to DOAB on : 2018-02-27 16:16:44
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Biotic and abiotic stress factors deliver a huge impact on plant life. Biotic stress factors such as damage through pathogens or herbivore attack, as well as abiotic stress factors like variation in temperature, rainfall and salinity, have placed the plant kingdom under constant challenges for survival. As a consequence, global agricultural and horticultural productivity has been disturbed to a large extent. Being sessile in nature, plants cannot escape from the stress, and instead adapt changes within their system to overcome the adverse conditions. These changes include physiological, developmental and biochemical alterations within the plant body which influences the genome, proteome and metabolome profiles of the plant. Since proteins are the ultimate players of cellular behavior, proteome level alterations during and recovery period of stress provide direct implications of plant responses towards stress factors. With current advancement of modern high-throughput technologies, much research has been carried out in this field. This e-book highlights the research and review articles that cover proteome level changes during the course or recovery period of various stress factors in plant life. Overall, the chapters in this e-book has provided a wealth of information on how plants deal with stress from a proteomics perspective.

Plant Organ Abscission: From Models to Crops

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889453283 Year: Pages: 271 DOI: 10.3389/978-2-88945-328-3 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Botany
Added to DOAB on : 2018-02-27 16:16:45
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Plant organ abscission is a developmental process regulated by the environment, stress, pathogens and the physiological status of the plant. In particular, seed and fruit abscission play an important role in seed dispersion and plant reproductive success and are common domestication traits with important agronomic consequences for many crop species. Indeed, in natural populations, shedding of the seed or fruit at the correct time is essential for reproductive success, while for crop species the premature or lack of abscission may be either beneficial or detrimental to crop productivity. The use of model plants, in particular Arabidopsis and tomato, have led to major advances in our understanding of the molecular and cellular mechanisms underlying organ abscission, and now many workers pursue the translation of these advances to crop species. Organ abscission involves specialized cell layers called the abscission zone (AZ), where abscission signals are perceived and cell separation takes place for the organ to be shed. A general model for plant organ abscission includes (1) the differentiation of the AZ, (2) the acquisition of AZ cells to become competent to respond to various abscission signals, (3) response to signals and the activation of the molecular and cellular processes that lead to cell separation in the AZ and (4) the post-abscission events related to protection of exposed cells after the organ has been shed. While this simple four-phase framework is helpful to describe the abscission process, the exact mechanisms of each stage, the differences between organ types and amongst diverse species, and in response to different abscission inducing signals are far from elucidated. For an organ to be shed, AZ cells must transduce a multitude of both endogenous and exogenous signals that lead to transcriptional and cellular and ultimately cell wall modifications necessary for adjacent cells to separate. How these key processes have been adapted during evolution to allow for organ abscission to take place in different locations and under different conditions is unknown. The aim of the current collection of articles is to present and be able to compare recent results on our understanding of organ abscission from model and crop species, and to provide a basis to understand both the evolution of abscission in plants and the translation of advances with model plants for applications in crop species.

Impact of Lipid Peroxidation on the Physiology and Pathophysiology of Cell Membranes

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889450824 Year: Pages: 88 DOI: 10.3389/978-2-88945-082-4 Language: English
Publisher: Frontiers Media SA
Subject: Physiology --- Science (General)
Added to DOAB on : 2017-07-06 13:27:36
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The general process of lipid peroxidation consists of three stages: initiation, propagation, and termination. The initiation phase of lipid peroxidation includes hydrogen atom abstraction. Several species can abstract the first hydrogen atom and include the radicals: hydroxyl, alkoxyl, peroxyl, and possibly HO* 2. The membrane lipids, mainly phospholipids, containing polyunsaturated fatty acids are predominantly susceptible to peroxidation because abstraction from a methylene group of a hydrogen atom, which contains only one electron, leaves at the back an unpaired electron on the carbon. The initial reaction of *OH with polyunsaturated fatty acids produces a lipid radical (L*), which in turn reacts with molecular oxygen to form a lipid hydroperoxide (LOOH). Further, the LOOH formed can suffer reductive cleavage by reduced metals, such as Fe++, producing lipid alkoxyl radical (LO*). Peroxidation of lipids can disturb the assembly of the membrane, causing changes in fluidity and permeability, alterations of ion transport and inhibition of metabolic processes. In addition, LOOH can break down, frequently in the presence of reduced metals or ascorbate, to reactive aldehyde products, including malondialdehyde (MDA), 4-hydroxy-2-nonenal (HNE), 4-hydroxy-2-hexenal (4-HHE) and acrolein. Lipid peroxidation is one of the major outcomes of free radical-mediated injury to tissue mainly because it can greatly alter the physicochemical properties of membrane lipid bilayers, resulting in severe cellular dysfunction. In addition, a variety of lipid by-products are produced as a consequence of lipid peroxidation, some of which can exert beneficial biological effects under normal physiological conditions. Intensive research performed over the last decades have also revealed that by-products of lipid peroxidation are also involved in cellular signalling and transduction pathways under physiological conditions, and regulate a variety of cellular functions, including normal aging. In the present collection of articles, both aspects (adverse and benefitial) of lipid peroxidation are illustrated in different biological paradigms. We expect this eBook may encourage readers to expand the current knowledge on the complexity of physiological and pathophysiological roles of lipid peroxidation.

Diacylglycerol Kinase Signalling

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889453351 Year: Pages: 96 DOI: 10.3389/978-2-88945-335-1 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Biology
Added to DOAB on : 2018-02-27 16:16:45
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Diacylglycerol kinases (DGKs) phosphorylate diacylglycerol (DG), catalyzing its conversion into phosphatidic acid (PA). This reaction attenuates membrane DG levels, limiting the localization/activation of signaling proteins that bind this lipid. Initially recognized as modulators of classical and novel PKC family members, the function of the DGK has further expanded with the identification of novel DG effectors including Ras Guanyl nucleotide-releasing proteins (RasGRP) and chimaerin Rac GTPases. The product of the DGK reaction, PA, is also a signaling lipid that mediates activation of multiple proteins including the mammalian target of rapamycin (mTOR). The DGK pathway thus modulates two lipids with important signaling properties that are also key intermediates in lipid metabolism and membrane trafficking. The DGK family in eukaryotes comprises 10 different members grouped into five different subfamilies characterized by the presence of particular regulatory motifs. These regions allow the different DGK isoforms to establish specific complexes and/or to be recruited to specific subcellular compartments. The subtle regulation of DG and PA catalyzed byspecific DGKs is sensed by a restricted set of molecules, providing the means for spatio-temporal regulation of signals in highly specialized cell systems.In the recent years, multiple studies have unveiled the functions of specific isoforms, their mechanisms of regulation and their participation in different pathways leading to and from DG and PA. Animal models have greatly helped to understand the specialized contribution of DGK mediated signals, particularly in the immune and central nervous systems. Mice deficient for individual DGK isoforms show defects in T and B cell functions, dendritic spine maintenance, osteoclast and mechanical-induced skeletal muscle formation. Studies in flies and worms link DGK mediated DAG metabolism with mTOR- mediated regulation of lifespan and stress responses. In plants DGK mediated PA formation contributes to plant responses to environmental signals.Aberrant DGK function has been recently associated with pathological states, an expected consequence of the essential role of these enzymes in the regulation of multiple tissue and systemic functions. DGK mutations/deletions have been related to human diseases including diabetes, atypical hemolytic-uremic syndrome, Parkinson disease and bipolar disorders. On the contrary DGK upregulation emerges as a non-oncogenic addition of certain tumors and represents one of the main mechanism by which cancer evades the immune attack. As a result, the DGK field emerges an exciting new area of research with important therapeutic potential.

The Role of Mitochondria, Oxidative Stress and Altered Calcium Homeostasis in Amyotrophic Lateral Sclerosis: From Current Developments in the Laboratory to Clinical Treatments

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889451463 Year: Pages: 336 DOI: 10.3389/978-2-88945-146-3 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2017-07-06 13:27:36
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Amyotrophic lateral sclerosis (ALS) is a rapidly progressive, devastating and fatal disease characterized by selective loss of upper and lower motor neurons of the cerebral cortex, brainstem, spinal cord and muscle atrophy. In spite of many years of research, the pathogenesis of ALS is still not well understood. ALS is a multifaceted genetic disease, in which genetic susceptibility to motor neuron death interacts with environmental factors and there is still no cure for this deleterious disease. At present, there is only one FDA approved drug, Riluzole which according to past studies only modestly slows the progression of the disease, and improves survival by up to three months. The suffering of the ALS patients, and their families is enormous and the economic burden is colossal. There is therefore a pressing need for new therapies. Different molecular pathways and pathological mechanisms have been implicated in ALS. According to past studies, altered calcium homeostasis, abnormal mitochondrial function, protein misfolding, axonal transport defects, excessive production of extracellular superoxide radicals, glutamate-mediated excitotoxicity, inflammatory events, and activation of oxidative stress pathways within the mitochondria and endoplasmic reticulum can act as major contributor that eventually leads to loss of connection between muscle and nerve ultimately resulting to ALS. However, the detailed molecular and cellular pathophysiological mechanisms and origin and temporal progression of the disease still remained elusive. Ongoing research and future advances will likely advance our improve understanding about various involved pathological mechanism ultimately leading to discoveries of new therapeutic cures. Importantly, clinical biomarkers of disease onset and progression are thus also urgently needed to support the development of the new therapeutic agents and novel preventive and curative strategies. Effective translation from pre-clinical to clinical studies will further require extensive knowledge regarding drug activity, bioavailability and efficacy in both the pre-clinical and clinical setting, and proof of biological activity in the target tissue. During the last decades, the development of new therapeutic molecules, advance neuroimaging tools, patient derived induced stem cells and new precision medicine approaches to study ALS has significantly improved our understanding of disease. In particular, new genetic tools, neuroimaging methods, cellular probes, biomarker study and molecular techniques that achieve high spatiotemporal resolution have revealed new details about the disease onset and its progression. In our effort to provide the interested reader, clinician and researchers a comprehensive summaries and new findings in this field of ALS research, hereby we have created this electronic book which comprises of twenty seven chapters having various reviews, perspective and original research articles. All these chapters and articles in this book not only summarize the cutting-edge techniques, approaches, cell and animal models to study ALS but also provide unprecedented coverage of the current developments and new hypothesis emerging in ALS research. Some examples are novel genetic and cell culture based models, mitochondria-mediated therapy, oxidative stress and ROS mechanism, development of stem cells and mechanism-based therapies as well as novel biomarkers for designing and testing effective therapeutic strategies that can benefit ALS patients who are at the earlier stages in the disease. I am extremely grateful to all the contributors to this book and want to thank them for their phenomenal efforts. Amyotrophic lateral sclerosis (ALS) is a rapidly progressive, devastating and fatal disease characterized by selective loss of upper and lower motor neurons of the cerebral cortex, brainstem, spinal cord and muscle atrophy. In spite of many years of research, the pathogenesis of ALS is still not well understood. ALS is a multifaceted genetic disease, in which genetic susceptibility to motor neuron death interacts with environmental factors and there is still no cure for this deleterious disease. At present, there is only one FDA approved drug, Riluzole which according to past studies only modestly slows the progression of the disease, and improves survival by up to three months. The suffering of the ALS patients, and their families is enormous and the economic burden is colossal. There is therefore a pressing need for new therapies. Different molecular pathways and pathological mechanisms have been implicated in ALS. According to past studies, altered calcium homeostasis, abnormal mitochondrial function, protein misfolding, axonal transport defects, excessive production of extracellular superoxide radicals, glutamate-mediated excitotoxicity, inflammatory events, and activation of oxidative stress pathways within the mitochondria and endoplasmic reticulum can act as major contributor that eventually leads to loss of connection between muscle and nerve ultimately resulting to ALS. However, the detailed molecular and cellular pathophysiological mechanisms and origin and temporal progression of the disease still remained elusive. Ongoing research and future advances will likely advance our improve understanding about various involved pathological mechanism ultimately leading to discoveries of new therapeutic cures. Importantly, clinical biomarkers of disease onset and progression are thus also urgently needed to support the development of the new therapeutic agents and novel preventive and curative strategies. Effective translation from pre-clinical to clinical studies will further require extensive knowledge regarding drug activity, bioavailability and efficacy in both the pre-clinical and clinical setting, and proof of biological activity in the target tissue. During the last decades, the development of new therapeutic molecules, advance neuroimaging tools, patient derived induced stem cells and new precision medicine approaches to study ALS has significantly improved our understanding of disease. In particular, new genetic tools, neuroimaging methods, cellular probes, biomarker study and molecular techniques that achieve high spatiotemporal resolution have revealed new details about the disease onset and its progression. In our effort to provide the interested reader, clinician and researchers a comprehensive summaries and new findings in this field of ALS research, hereby we have created this electronic book which comprises of twenty seven chapters having various reviews, perspective and original research articles. All these chapters and articles in this book not only summarize the cutting-edge techniques, approaches, cell and animal models to study ALS but also provide unprecedented coverage of the current developments and new hypothesis emerging in ALS research. Some examples are novel genetic and cell culture based models, mitochondria-mediated therapy, oxidative stress and ROS mechanism, development of stem cells and mechanism-based therapies as well as novel biomarkers for designing and testing effective therapeutic strategies that can benefit ALS patients who are at the earlier stages in the disease. I am extremely grateful to all the contributors to this book and want to thank them for their phenomenal efforts.

Mitochondria: Hubs of Cellular Signaling, Energetics and Redox Balance

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889452392 Year: Pages: 228 DOI: 10.3389/978-2-88945-239-2 Language: English
Publisher: Frontiers Media SA
Subject: Physiology --- Science (General)
Added to DOAB on : 2017-10-13 14:57:01
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Poised at the convergence of most catabolic and anabolic pathways, mitochondria are the center of heterotrophic aerobic life, representing a hub in the overall metabolic network of cells. The energetic functions performed by mitochondria face the unavoidable redox hurdle of handling huge amounts of oxygen while keeping its own as well as the cellular redox environment under control. Reactive oxygen species (ROS) are produced in the respiratory chain as a result of the energy supplying function of mitochondria. Originally considered an unavoidable by-product of oxidative phosphorylation, ROS have become crucial signaling molecules when their levels are kept within physiological range. This occurs when their production and scavenging are balanced within mitochondria and cells. Mitochondria-generated hydrogen peroxide can act as a signaling molecule within mitochondria or in the cytoplasm, affecting multiple networks that control, for example, cell cycle, stress response, cell migration and adhesion, energy metabolism, redox balance, cell contraction, and ion channels. However, under pathophysiological conditions, excessive ROS levels can happen due to either overproduction, overwhelming of antioxidant defenses, or both. Under oxidative stress, detrimental effects of ROS include oxidation of protein, lipids, and nucleic acids; mitochondrial depolarization and calcium overload; and cell-wide oscillations mediated by ROS-induced ROS release mechanisms. Mitochondrial dysfunction is central in the pathogenesis of numerous human maladies including cardiomyopathies and neurodegeneration. Diseases characterized by altered nutrient metabolism, such as diabetes and cancer, exhibit elevated ROS levels. These may contribute to pathogenesis by increasing DNA mutation, affecting regulatory signaling and transcription, and promoting inflammation. Under metabolic stress, several ionic channels present in the inner and outer mitochondrial membranes can have pro-life and -death effects. In the present E-book, based on the Frontiers Research Topic entitled: "Mitochondria: Hubs of cellular signaling, energetics and redox balance", we address one of the fundamental questions that the field of ROS biology faces today: how do mitochondria accomplish a reliable energy provision and at the same time keep ROS levels within physiological, non-harming, limits but crucial for cellular signaling function? Additionally, and within the perspective of mitochondria as signaling-energetic hubs in the extensive cellular metabolic network, we ask how can their collective dynamics scale from the subcellular to the cellular, tissue and organ levels to affect function in health and disease.

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