Sarcopenia, the age-related decline in muscle mass and function, derives from multiple etiological mechanisms. Accumulative research suggests that reactive oxygen species (ROS) generation plays a critical role in the development of this pathophysiological disorder. In this communication, we review the various signaling pathways that control muscle metabolic and functional integrity such as protein turnover, cell death and regeneration, inflammation, organismic damage, and metabolic functions. Although no single pathway can be identified as the most crucial factor that causes sarcopenia, age-associated dysregulation of redox signaling appears to underlie many deteriorations at physiological, subcellular, and molecular levels. Furthermore, discord of mitochondrial homeostasis with aging affects most observed problems and requires our attention. The search for the primary suspect of the fundamental mechanism for sarcopenia will likely take more intense research for the secret of this health hazard to the elderly to be unlocked.
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http://dx.doi.org/10.3390/ijms22169045 | DOI Listing |
Cell Signal
January 2025
Institute of Medical Science, Ajou University School of Medicine, Suwon, Gyeonggi 16499, Republic of Korea; Department of Biomedical Sciences, Ajou University Graduate School of Medicine, Suwon, Gyeonggi 16499, Republic of Korea. Electronic address:
Oxidative stress caused by reactive oxygen species (ROS) and superoxides is linked to various cancer-related biological events. Extracellular superoxide dismutase (SOD3), an antioxidant enzyme that removes superoxides, contributes to redox homeostasis and has the potential to regulate tumorigenesis. Histone deacetylase 6 (HDAC6), a major HDAC isoform responsible for mediating the deacetylation of non-histone protein substrates, also plays a role in cancer progression.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
the University of Texas at Austin, Austin, TX, USA.
Background: Imbalanced Fe levels can lead to oxidative stress and initiate ferroptosis, an Fe-dependent cell death that involves lipid peroxidation and can lead to neuron cell loss in neurodegenerative diseases including Alzheimer's disease (AD). While the Fe/Fe ratio has been identified as the primary determining factor for lipid peroxidation, the role of Fe redox equilibrium and dynamic in AD is not well understood, due to limited tools for visualizing Fe and Fe simultaneously. To overcome this limitation, we recently reported DNAzyme-based sensors for simultaneous imaging of Fe and Fe.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Ecole polytechnique - CNRS UMR7654, Palaiseau, Ile-de-France, France; Université Paris Cité - Inserm UMR-S1124, Paris, Ile-de-France, France.
Alzheimer's disease (AD) is the most common dementia in humans that today concerns 50 million individuals worldwide and will affect more than 100 million people in 2050. Except for familial AD cases (<5% of AD patients) for which AD pathology connects to mutations in critical genes involved in the processing of the amyloid precursor protein into neurotoxic Aß peptides, it remains unknown what provokes the overproduction and deposition of Aß peptides in the brain of sporadic AD cases (>95% of AD patients). Some nanosized materials, e.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Neuroscience Graduate Program, Weill Cornell Medicine, New York, NY, USA.
Background: Mitochondrial reactive oxygen species (mROS), such as superoxide and hydrogen peroxide (HO), are implicated in aging-associated neurological disorders, including Alzheimer's Disease and frontotemporal dementia. Mitochondrial complex III of the respiratory chain has the highest capacity for mROS production and generates mROS toward the cytosol, poising it to regulate intracellular signaling and disease mechanisms. However, the exact triggers of complex III-derived ROS (CIII-ROS), its downstream molecular targets, and its functional roles in dementia-related pathogenesis remain unclear.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Sapienza University of Rome, Rome, Rome, Italy.
Background: Brain insulin resistance (bIR) heavily impacts on the core pathological processes of aging and Alzheimer disease (AD) since insulin regulates brain metabolism and cognitive functions. A close link among bIR, oxidative stress (OS) and mitochondrial defects exists, that contributes to brain dysfunctions observed in AD. Intriguingly, several studies suggest that intranasal insulin treatment (INI) enhances cognitive performance and reduced AD neuropathology both in humans and murine models of AD.
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