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

Authors: --- ---
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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Abstract

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.

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

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