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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.

Atrophy --- Mitochondria --- mitophagy --- nutrition --- Aging --- muscle contractility --- skeletal muscle --- Metabolism --- Hypertrophy --- mitochondrial dynamics

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The kidney performs important functions in the human body and can inflict either acute kidney injury (AKI) or chronic kidney disease (CKD). AKI can be induced by kidney ischemia, drugs such as cisplatin, and heavy metals such as cadmium and arsenic. CKD can be induced by drugs, heavy metals, hypertension, and diabetes, as well as cancer. Importantly, nearly all kidney disorders have been shown to involve redox imbalance, reductive stress, oxidative stress, and mitochondrial abnormalities such as impaired mitochondrial homeostasis, including disrupted mitophagy and deranged mitochondrial unfolded protein responses. Understanding how these redox-related dysregulated pathways operate may give us new insights into how to design novel approaches to fighting kidney disease. This Special Issue of Biomolecules entitled “Redox imbalance and mitochondrial abnormalities in kidney disease” covers a variety of topics focusing on oxidative stress, mitochondrial dysfunction, and antioxidation enhancement implicated in kidney disease or kidney transplantation.

diabetic kidney disease --- caloric restriction --- NADH/NAD+ --- redox imbalance --- mitochondrial homeostasis --- mitophagy --- oxidative stress --- kidney allograft --- kidney rejection --- ischemia --- acute kidney injury (AKI) --- chronic kidney disease (CKD) --- tricarboxylic acid (TCA) cycle --- mitochondrial metabolism --- mitochondrial redox signaling --- mitochondrial proteins --- oxidative phosphorylation (OXPHOS) --- fatty acid (FA) β-oxidation --- mitochondrial dynamics --- biogenesis --- diabetes --- kidney --- mitochondria --- Oryza sativa --- rice husk --- TCA cycle metabolites --- kidney diseases --- renalase --- chronic kidney disease --- major adverse cardiovascular outcomes --- cadmium --- kidney injury --- renal toxicity --- oxidative damage --- proximal tubule --- controlled oxygenated rewarming --- mitochondrial uncoupling --- rewarming injury --- temperature paradox --- redox --- mitochondrial dysfunction --- SGLT2 --- mitochondrial reactive oxygen species --- Warburg effect --- podocytopathies --- mitochondrial oxidative stress --- reactive oxygen species (ROS) --- antioxidant defense --- cell death --- n/a

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Mitochondria are the powerhouses of cells; however, mitochondrial dysfunction causes energy depletion and cell death in a variety of diseases. Altered oxidative phosphorylation and ion homeostasis are associated with ROS production resulting from the disassembly of respiratory supercomplexes and the disruption of electron transfer chains. In pathological conditions, the dysregulation of mitochondrial homeostasis promotes Ca2+ overload in the matrix and ROS accumulation, which induces the mitochondrial permeability transition pore formation responsible for mitochondrial morphological changes linked to membrane dynamics, and ultimately, cell death. Finally, studies on the impaired mitochondrial bioenergetics in pathology could provide molecular tools to counteract diseases associated with mitochondrial dysfunction.

aging heart --- Bcl-2 family --- mitochondria --- programmed cell death --- fatty acid oxidation --- palmitate --- oleate --- m.3243A&gt --- G mutation --- MT-ATP6 --- m.8909T&gt --- C --- ATP synthase --- nephropathy --- oxidative phosphorylation --- mitochondrial disease --- cardiolipin --- Barth syndrome --- Sengers syndrome --- respiratory chain --- Dilated Cardiomyopathy with Ataxia --- cardiomyopathy --- mammalian complex I --- NADH dehydrogenase --- complex I assembly --- complex I structure --- complex I deficiency --- supernumerary subunits --- electron transport chain --- mitochondrial dysfunction --- Leigh syndrome --- mitochondrial diseases --- yeast --- Saccharomyces cerevisiae --- pet mutants --- pancreatic endocrine cells --- mathematical model --- cellular bioenergetics --- diabetes --- glucagon --- insulin --- exercise --- immune system --- metabolic disease --- COVID-19 --- mitochondrial dynamics --- viral infections --- MAVS --- RIG-I --- MDA5 --- innate immune response --- SARS CoV-2 --- RSV --- influenza --- respiratory supercomplexes --- ROS --- ATP synthase/hydrolase --- mitochondrial permeability transition pore --- cristae --- cellular signaling --- human disease --- mitochondrial dynamic --- cell signaling --- cancer --- respiratory complexes --- oxidative stress --- mitochondrial DNA --- MTCYB mutations --- cytochrome b --- complex III --- aging --- energy metabolism --- entorhinal cortex --- lipoxidation-derived damage --- neurodegeneration --- oxidative damage --- protein import --- respiratory complex assembly --- supercomplexes --- mitochondrial proteostasis --- heart failure --- bioenergetics --- assembly factor --- atypical myopathy --- high-resolution respirometry --- toxicity assays --- cell culture --- equine primary myoblasts --- fibroblasts --- frozen tissue --- leukocytes --- oxygen consumption --- platelets --- respirometry --- skeletal muscle --- n/a

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The book is a collection of original research and review articles addressing the intriguing field of the cellular and molecular players involved in muscle homeostasis and regeneration. One of the most ambitious aspirations of modern medical science is the possibility of regenerating any damaged part of the body, including skeletal muscle. This desire has prompted clinicians and researchers to search for innovative technologies aimed at replacing organs and tissues that are compromised. In this context, the papers, collected in this book, addressing a specific aspects of muscle homeostasis and regeneration under physiopathologic conditions, will help us to better understand the underlying mechanisms of muscle healing and will help to design more appropriate therapeutic approaches to improve muscle regeneration and to counteract muscle diseases.

lysine --- mTORC1 --- satellite cells --- proliferation --- skeletal muscle growth --- muscle satellite cell --- transthyretin --- thyroid hormone --- myogenesis --- exosomes --- skeletal muscle --- genotype --- genetic variation --- muscle phenotypes --- sarcopenia --- aging --- calcium homeostasis --- hibernation --- mitochondria --- sarcoplasmic reticulum --- Acvr1b --- Tgfbr1 --- myostatin --- Col1a1 --- fibrosis --- atrophy --- IGF2R --- muscle homeostasis --- inflammation --- muscular dystrophy --- pericytes --- macrophages --- Nfix --- phagocytosis --- RhoA-ROCK1 --- splicing isoforms --- CRISPR-Cas9 --- exon deletion --- NF-Y --- muscle differentiation --- C2C12 cells --- denervation --- neuromuscular junction --- heavy resistance exercise --- acetylcholine receptor --- cell culture --- neonatal myosin --- neural cell adhesion molecule --- biomarkers --- mitophagy --- mitochondrial dynamics --- mitochondrial quality control --- mitochondrial-derived vesicles (MDVs) --- mitochondrial-lysosomal axis --- Hibernation --- electron microscopy --- immunocytochemistry --- α-smooth muscle actin --- confocal microscopy --- connexin 43 --- connexin 26 --- gap junctions --- myofibroblasts --- Platelet-Rich Plasma --- transforming growth factor (TGF)-β1 --- muscle regeneration --- inflammatory response --- cell precursors --- experimental methods --- stem cell markers --- muscles --- heterotopic ossification --- skeletal muscle stem and progenitor cells --- HO precursors --- muscle atrophy --- septicemia --- mitochondrial fusion --- mitochondrial fission --- iPSC --- extracellular vesicles --- Drosophila --- muscle --- genetic control --- muscle diversification --- fascicle --- myofiber --- myofibril --- sarcomere --- hypertrophy --- hyperplasia --- splitting --- radial growth --- longitudinal growth --- exercise --- muscle stem cells --- stem cells niche --- neuromuscular disorders --- Duchenne muscular dystrophy --- pharmacological approach --- single-cell --- mass cytometry --- skeletal muscle regeneration --- skeletal muscle homeostasis --- fibro/adipogenic progenitors --- myogenic progenitors --- muscle populations --- evolution --- metazoans --- differentiation --- transdifferentiation --- muscle precursors --- regenerative medicine --- stem cells --- FAPs --- tissue niche --- growth factors --- muscle pathology