@article{JohannKleinertKlaus2021,
  author    = {Johann, Kornelia and Kleinert, Maximilian and Klaus, Susanne},
  title     = {The role of GDF15 as a myomitokine},
  series = {Cells},
  volume    = {10},
  journal   = {Cells},
  number    = {11},
  publisher = {MDPI},
  address   = {Basel},
  issn      = {2073-4409},
  doi       = {10.3390/cells10112990},
  pages     = {16},
  year      = {2021},
  abstract  = {Growth differentiation factor 15 (GDF15) is a cytokine best known for affecting systemic energy metabolism through its anorectic action. GDF15 expression and secretion from various organs and tissues is induced in different physiological and pathophysiological states, often linked to mitochondrial stress, leading to highly variable circulating GDF15 levels. In skeletal muscle and the heart, the basal expression of GDF15 is very low compared to other organs, but GDF15 expression and secretion can be induced in various stress conditions, such as intense exercise and acute myocardial infarction, respectively. GDF15 is thus considered as a myokine and cardiokine. GFRAL, the exclusive receptor for GDF15, is expressed in hindbrain neurons and activation of the GDF15-GFRAL pathway is linked to an increased sympathetic outflow and possibly an activation of the hypothalamic-pituitary-adrenal (HPA) stress axis. There is also evidence for peripheral, direct effects of GDF15 on adipose tissue lipolysis and possible autocrine cardiac effects. Metabolic and behavioral outcomes of GDF15 signaling can be beneficial or detrimental, likely depending on the magnitude and duration of the GDF15 signal. This is especially apparent for GDF15 production in muscle, which can be induced both by exercise and by muscle disease states such as sarcopenia and mitochondrial myopathy.},
  language  = {en}
}
@article{SackFerrariFriesenetal.2022,
  author    = {Sack, Carolin and Ferrari, Nina and Friesen, David and Haas, Fabiola and Klaudius, Marlen and Schmidt, Lisa and Torbahn, Gabriel and Wulff, Hagen and Joisten, Christine},
  title     = {Health risks of sarcopenic obesity in overweight children and adolescents: data from the CHILT III Programme (Cologne)},
  series = {Journal of Clinical Medicine : open access journal},
  volume    = {11},
  journal   = {Journal of Clinical Medicine : open access journal},
  number    = {1},
  publisher = {MDPI},
  address   = {Basel},
  issn      = {2077-0383},
  doi       = {10.3390/jcm11010277},
  pages     = {12},
  year      = {2022},
  abstract  = {Sarcopenic obesity is increasingly found in youth, but its health consequences remain unclear. Therefore, we studied the prevalence of sarcopenia and its association with cardiometabolic risk factors as well as muscular and cardiorespiratory fitness using data from the German Children's Health InterventionaL Trial (CHILT III) programme. In addition to anthropometric data and blood pressure, muscle and fat mass were determined with bioelectrical impedance analysis. Sarcopenia was classified via muscle-to-fat ratio. A fasting blood sample was taken, muscular fitness was determined using the standing long jump, and cardiorespiratory fitness was determined using bicycle ergometry. Of the 119 obese participants included in the analysis (47.1\% female, mean age 12.2 years), 83 (69.7\%) had sarcopenia. Affected individuals had higher gamma-glutamyl transferase, higher glutamate pyruvate transaminase, higher high-sensitivity C-reactive protein, higher diastolic blood pressure, and lower muscular and cardiorespiratory fitness (each p < 0.05) compared to participants who were 'only' obese. No differences were found in other parameters. In our study, sarcopenic obesity was associated with various disorders in children and adolescents. However, the clinical value must be tested with larger samples and reference populations to develop a unique definition and appropriate methods in terms of identification but also related preventive or therapeutic approaches.},
  language  = {en}
}
@phdthesis{LopesFernando2023,
  author    = {Lopes Fernando, Raquel Sofia},
  title     = {The impact of aging on proteolytic systems, transcriptome and metabolome of slow and fast muscle fiber types},
  doi       = {10.25932/publishup-60579},
  school      = {Universit{\"a}t Potsdam},
  pages     = {XI, 125},
  year      = {2023},
  abstract  = {Aging is a complex process characterized by several factors, including loss of genetic and epigenetic information, accumulation of chronic oxidative stress, protein damage and aggregates and it is becoming an emergent drug target. Therefore, it is the utmost importance to study aging and agerelated diseases, to provide treatments to develop a healthy aging process. Skeletal muscle is one of the earliest tissues affected by age-related changes with progressive loss of muscle mass and function from 30 years old, effect known as sarcopenia. Several studies have shown the accumulation of protein aggregates in different animal models, as well as in humans, suggesting impaired proteostasis, a hallmark of aging, especially regarding degradation systems. Thus, different publications have explored the role of the main proteolytic systems in skeletal muscle from rodents and humans, like ubiquitin proteasomal system (UPS) and autophagy lysosomal system (ALS), however with contradictory results. Yet, most of the published studies are performed in muscles that comprise more than one fiber type, that means, muscles composed by slow and fast fibers. These fiber types, exhibit different metabolism and contraction speed; the slow fibers or type I display an oxidative metabolism, while fast fibers function towards a glycolytic metabolism ranging from fast oxidative to fast glycolytic fibers. To this extent, the aim of this thesis sought to understand on how aging impacts both fiber types not only regarding proteostasis but also at a metabolome and transcriptome network levels. Therefore, the first part of this thesis, presents the differences between slow oxidative (from Soleus muscle) and fast glycolytic fibers (Extensor digitorum longus, EDL) in terms of degradation systems and how they cope with oxidative stress during aging, while the second part explores the differences between young and old EDL muscle transcriptome and metabolome, unraveling molecular features. More specifically, the results from the present work show that slow oxidative muscle performs better at maintaining the function of UPS and ALS during aging than EDL muscle, which is clearly affected, accounting for the decline in the catalytic activity rates and accumulation of autophagy-related proteins. Strinkingly, transcriptome and metabolome analyses reveal that fast glycolytic muscle evidences significant downregulation of mitochondrial related processes and damaged mitochondria morphology during aging, despite of having a lower oxidative metabolism compared to oxidative fibers. Moreover, predictive analyses reveal a negative association between aged EDL gene signature and lifespan extending interventions such as caloric restriction (CR). Although, CR intervention does not alter the levels of mitochondrial markers in aged EDL muscle, it can reverse the higher mRNA levels of muscle damage markers. Together, the results from this thesis give new insights about how different metabolic muscle fibers cope with age-related changes and why fast glycolytic fibers are more susceptible to aging than slow oxidative fibers.},
  language  = {en}
}