@article{HeWuertzKozakKuehletal.2021,
  author    = {He, Yangyang and W{\"u}rtz-Kozak, Karin and K{\"u}hl, Linn Kristina and Wippert, Pia-Maria},
  title     = {Extracellular vesicles},
  series = {International journal of molecular sciences},
  volume    = {22},
  journal   = {International journal of molecular sciences},
  number    = {11},
  publisher = {Molecular Diversity Preservation International},
  address   = {Basel},
  issn      = {1422-0067},
  doi       = {10.3390/ijms22115846},
  pages     = {15},
  year      = {2021},
  abstract  = {Osteoporosis is characterized by low bone mass and damage to the bone tissue's microarchitecture, leading to increased fracture risk. Several studies have provided evidence for associations between psychosocial stress and osteoporosis through various pathways, including the hypothalamic-pituitary-adrenocortical axis, the sympathetic nervous system, and other endocrine factors. As psychosocial stress provokes oxidative cellular stress with consequences for mitochondrial function and cell signaling (e.g., gene expression, inflammation), it is of interest whether extracellular vesicles (EVs) may be a relevant biomarker in this context or act by transporting substances. EVs are intercellular communicators, transfer substances encapsulated in them, modify the phenotype and function of target cells, mediate cell-cell communication, and, therefore, have critical applications in disease progression and clinical diagnosis and therapy. This review summarizes the characteristics of EVs, their role in stress and osteoporosis, and their benefit as biological markers. We demonstrate that EVs are potential mediators of psychosocial stress and osteoporosis and may be beneficial in innovative research settings.},
  language  = {en}
}
@article{SchmidtKorbAbell2017,
  author    = {Schmidt, Marco F. and Korb, Oliver and Abell, Chris},
  title     = {Antagonists of the miRNA-Argonaute 2 Protein Complex},
  series = {Drug Target miRNA: Methods and Protocols},
  volume    = {1517},
  journal   = {Drug Target miRNA: Methods and Protocols},
  publisher = {Springer},
  address   = {New York},
  isbn      = {978-1-4939-6563-2},
  issn      = {1064-3745},
  doi       = {10.1007/978-1-4939-6563-2_17},
  pages     = {239 -- 249},
  year      = {2017},
  abstract  = {microRNAs (miRNAs) have been identified as high-value drug targets. A widely applied strategy in miRNA inhibition is the use of antisense agents. However, it has been shown that oligonucleotides are poorly cell permeable because of their complex chemical structure and due to their negatively charged backbone. Consequently, the general application of oligonucleotides in therapy is limited. Since miRNAs' functions are executed exclusively by the Argonaute 2 protein, we therefore describe a protocol for the design of a novel miRNA inhibitor class: antagonists of the miRNA-Argonaute 2 protein complex, so-called anti-miR-AGOs, that not only block the crucial binding site of the target miRNA but also bind to the protein's active site. Due to their lower molecular weight and, thus, more drug-like chemical structure, the novel inhibitor class may show better pharmacokinetic properties than reported oligonucleotide inhibitors, enabling them for potential therapeutic use.},
  language  = {en}
}