1,721,037 research outputs found
FGF21: a promising therapeutic agent for alcoholic cardiomyopathy?†
No full textThe metabolic regulator fibroblast growth factor 21 (FGF21) has been reported as a cardioprotective factor regulating cardiac remodeling in several cardiac diseases. In a recent issue of The Journal of Pathology, Ferrer-Curriu, Guitart-Mampel et al investigated FGF21 in alcoholic cardiomyopathy (ACM). They showed that FGF21 deficiency aggravates alcohol-induced cardiac damage and dysfunction by exacerbating mitochondrial alterations, oxidative stress, and lipid metabolic dysregulation, suggesting FGF21 as a promising therapeutic agent in ACM. Paradoxically, FGF21 cardiac and circulating levels correlate with cardiac damage and oxidative stress in patients with ACM, pointing to FGF21 as a potential biomarker of alcohol-induced cardiac damage. Further studies are needed to address when FGF21 can be used as a diagnostic biomarker and when it can be used as a therapeutic agent to treat ACM. © 2021 The Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd
Implications of mitochondrial fusion and fission in skeletal muscle mass and health
No full textThe continuous dynamic reshaping of mitochondria by fusion and fission events is critical to keep mitochondrial quality and function under control in response to changes in energy and stress. Maintaining a functional, highly interconnected mitochondrial reticulum ensures rapid energy production and distribution. Moreover, mitochondrial networks act as dynamic signaling hub to adapt to the metabolic demands imposed by contraction, energy expenditure, and general metabolism. However, excessive mitochondrial fusion or fission results in the disruption of the skeletal muscle mitochondrial network integrity and activates a retrograde response from mitochondria to the nucleus, leading to muscle atrophy, weakness and influencing whole-body homeostasis. These actions are mediated via the secretion of mitochondrial-stress myokines such as FGF21 and GDF15. Here we will summarize recent discoveries in the role of mitochondrial fusion and fission in the control of muscle mass and in regulating physiological homeostasis and disease progression
The connection between the dynamic remodeling of the mitochondrial network and the regulation of muscle mass
Full text linkThe dynamic coordination of processes controlling the quality of the mitochondrial network is crucial to maintain the function of mitochondria in skeletal muscle. Changes of mitochondrial proteolytic system, dynamics (fusion/fission), and mitophagy induce pathways that affect muscle mass and performance. When muscle mass is lost, the risk of disease onset and premature death is dramatically increased. For instance, poor quality of muscles correlates with the onset progression of several age-related disorders such as diabetes, obesity, cancer, and aging sarcopenia. To date, there are no drug therapies to reverse muscle loss, and exercise remains the best approach to improve mitochondrial health and to slow atrophy in several diseases. This review will describe the principal mechanisms that control mitochondrial quality and the pathways that link mitochondrial dysfunction to muscle mass regulation
The authors reply: Letter on: "Fibroblast growth factor 21 controls mitophagy and muscle mass" by Oost et al
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I Reattori Nucleari ad Alta Temperatura (HTR) nella Prospettiva Energetica Futura
No full textPubblicato sul Portale dell'Ingegneria Energetica e Nuclear
Produzione di H2 per Via Nucleare mediante Steam Reforming
No full textPortale dell'Ingegneria Energetica e Nuclear
Il Reattore Nucleare Naturale di Oklo
No full textPubblicato sul Portale dell'Ingegneria Energetica e Nuclear
Mitochondrial Biogenesis and Fragmentation as Regulators of Muscle Protein Degradation
No full textMitochondria form a dynamic network that rapidly adapts to cellular energy demand. This adaptation is particularly important in skeletal muscle because of its high metabolic rate. Indeed, muscle energy level is one of the cellular checkpoints that lead either to sustained protein synthesis and growth or protein breakdown and atrophy. Mitochondrial function is affected by changes in shape, number, and localization. The dynamics that control the mitochondrial network, such as biogenesis and fusion, or fragmentation and fission, ultimately affect the signaling pathways that regulate muscle mass. Regular exercise and healthy muscles are important players in the metabolic control of human body. Indeed, a sedentary lifestyle is detrimental for muscle function and is one of the major causes of metabolic disorders such as obesity and diabetes. This article reviews the rapid progress made in the past few years regarding the role of mitochondria in the control of proteolytic systems and in the loss of muscle mass and function
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