Author Correction: Age-related mitochondrial alterations in brain and skeletal muscle of the YAC128 model of Huntington disease

Sarcopenia is defined by the age-related loss of skeletal muscle quality, which relies on mitochondrial homeostasis. During aging, several mitochondrial features such as bioenergetics, dynamics, biogenesis, and selective autophagy (mitophagy) are altered and impinge on protein homeostasis, resulting in loss of muscle mass and function. Thus, mitochondrial dysfunction contributes significantly to the complex pathogenesis of sarcopenia, and mitochondria are indicated as potential targets to prevent and treat this age-related condition. After a concise presentation of the age-related modifications in skeletal muscle quality and mitochondrial homeostasis, the present review summarizes the most relevant findings related to mitochondrial alterations in sarcopenia.

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Age-related impairment of muscle resident progenitor cells affect the metabolic homeostasis of skeletal muscle

10.1055/s-0037-1603536 ◽

2017 ◽

Author(s):

F Garcia ◽

AM Jank ◽

TJ Schulz

Keyword(s):

Skeletal Muscle ◽

Progenitor Cells ◽

Metabolic Homeostasis ◽

Age Related

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NAD+ supplementation normalises central carbon metabolism in skeletal muscle: a mechanistic insight into the energetic consequences of age-related NAD+ decline

Endocrine Abstracts ◽

10.1530/endoabs.44.p187 ◽

2016 ◽

Author(s):

Lucy Oldacre-Bartley ◽

Rachel Fletcher ◽

Kate Hollinshead ◽

Yasir Elhassan ◽

Craig Doig ◽

...

Keyword(s):

Skeletal Muscle ◽

Carbon Metabolism ◽

Central Carbon Metabolism ◽

Mechanistic Insight ◽

Age Related ◽

Central Carbon ◽

Insight Into

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Age-Related Mitochondrial Alterations without Neuronal Loss in the Hippocampus of a Transgenic Model of Alzheimer's Disease

Current Alzheimer Research ◽

10.2174/1567205011310040005 ◽

2013 ◽

Vol 10 (4) ◽

pp. 390-405 ◽

Cited By ~ 18

Author(s):

Mar Cuadrado-Tejedor ◽

Jesus Felipe Cabodevilla ◽

Marta Zamarbide ◽

Teresa Gomez-Isla ◽

Rafael Franco ◽

...

Keyword(s):

Neuronal Loss ◽

Transgenic Model ◽

Mitochondrial Alterations ◽

Age Related

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Molecular Mechanism and Pathogenesis of Sarcopenia: An Overview

International Journal of Molecular Sciences ◽

10.3390/ijms22063032 ◽

2021 ◽

Vol 22 (6) ◽

pp. 3032

Author(s):

Anna Picca ◽

Riccardo Calvani

Keyword(s):

Skeletal Muscle ◽

Molecular Mechanism ◽

Muscle Mass ◽

Skeletal Muscle Mass ◽

Strength Function ◽

Age Related

Sarcopenia involves a progressive age‐related decline of skeletal muscle mass and strength/function [...]

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Gait disturbances and muscle dysfunction in fibroblast growth factor 2 knockout mice

Scientific Reports ◽

10.1038/s41598-021-90565-0 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

C. Homer-Bouthiette ◽

L. Xiao ◽

Marja M. Hurley

Keyword(s):

Skeletal Muscle ◽

Growth Factor ◽

Muscle Strength ◽

Fibroblast Growth Factor ◽

Muscle Function ◽

Fibroblast Growth Factor 2 ◽

Fibroblast Growth ◽

Skeletal Muscle Function ◽

Age Related ◽

Gait Disturbances

AbstractFibroblast growth factor 2 (FGF2) is important in musculoskeletal homeostasis, therefore the impact of reduction or Fgf2 knockout on skeletal muscle function and phenotype was determined. Gait analysis as well as muscle strength testing in young and old WT and Fgf2KO demonstrated age-related gait disturbances and reduction in muscle strength that were exacerbated in the KO condition. Fgf2 mRNA and protein were significantly decreased in skeletal muscle of old WT compared with young WT. Muscle fiber cross-sectional area was significantly reduced with increased fibrosis and inflammatory infiltrates in old WT and Fgf2KO vs. young WT. Inflammatory cells were further significantly increased in old Fgf2KO compared with old WT. Lipid-related genes and intramuscular fat was increased in old WT and old Fgf2KO with a further increase in fibro-adipocytes in old Fgf2KO compared with old WT. Impaired FGF signaling including Increased β-Klotho, Fgf21 mRNA, FGF21 protein, phosphorylated FGF receptors 1 and 3, was observed in old WT and old Fgf2KO. MAPK/ ERK1/2 was significantly increased in young and old Fgf2KO. We conclude that Fgf2KO, age-related decreased FGF2 in WT mice, and increased FGF21 in the setting of impaired Fgf2 expression likely contribute to impaired skeletal muscle function and sarcopenia in mice.

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Apoptosis in the Extraosseous Calcification Process

Cells ◽

10.3390/cells10010131 ◽

2021 ◽

Vol 10 (1) ◽

pp. 131

Author(s):

Federica Boraldi ◽

Francesco Demetrio Lofaro ◽

Daniela Quaglino

Keyword(s):

Genetic Basis ◽

Membrane Vesicles ◽

Matrix Vesicles ◽

Apoptotic Bodies ◽

Connective Tissues ◽

Mineralization Process ◽

Mitochondrial Alterations ◽

Age Related ◽

And Oxidative Stress ◽

And Cartilage

Extraosseous calcification is a pathologic mineralization process occurring in soft connective tissues (e.g., skin, vessels, tendons, and cartilage). It can take place on a genetic basis or as a consequence of acquired chronic diseases. In this last case, the etiology is multifactorial, including both extra- and intracellular mechanisms, such as the formation of membrane vesicles (e.g., matrix vesicles and apoptotic bodies), mitochondrial alterations, and oxidative stress. This review is an overview of extraosseous calcification mechanisms focusing on the relationships between apoptosis and mineralization in cartilage and vascular tissues, as these are the two tissues mostly affected by a number of age-related diseases having a progressively increased impact in Western Countries.

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