@phdthesis{He2023,
  author    = {He, Yangyang},
  title     = {Extracellular vesicles as the potential mediators of psychosocial stress contribution to osteoporosis},
  doi       = {10.25932/publishup-59437},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-594372},
  school      = {Universit{\"a}t Potsdam},
  pages     = {70},
  year      = {2023},
  abstract  = {Background: The characteristics of osteoporosis are decreased bone mass and destruction towards the microarchitecture of bone tissue, which raises the risk of fracture. Psychosocialstress and osteoporosis are linked by sympathetic nervous system, hypothalamic-pituitary-adrenal axis, and other endocrine factors. Psychosocial stress causes a series of effects on the organism, and this long-term depletion at the cellular level is considered to be mitochondrial allostatic load, including mitochondrial dysfunction and oxidative stress. Extracellular vesicles (EVs) are involved in the mitochondrial allostatic load process and may as biomarkers in this setting. As critical participants during cell-to-cell communications, EVs serve as transport vehicles for nucleic acid and proteins, alter the phenotypic and functional characteristics of their target cells, and promote cell-to-cell contact. And hence, they play a significant role in the diagnosis and therapy of many diseases, such as osteoporosis. Aim: This narrative review attempts to outline the features of EVs, investigate their involvement in both psychosocial stress and osteoporosis, and analyze if EVs can be potential mediators between both. Methods: The online database from PubMed, Google Scholar, and Science Direct were searched for keywords related to the main topic of this study, and the availability of all the selected studies was verified. Afterward, the findings from the articles were summarized and synthesized. Results: Psychosocial stress affects bone remodeling through increased neurotransmitters such as glucocorticoids and catecholamines, as well as increased glucose metabolism. Furthermore, psychosocial stress leads to mitochondrial allostatic load, including oxidative stress, which may affect bone remodeling. In vitro and in vivo data suggest EVs might involve in the link between psychosocial stress and bone remodeling through the transfer of bioactive substances and thus be a potential mediator of psychosocial stress leading to osteoporosis. Conclusions: According to the included studies, psychosocial stress affects bone remodeling, leading to osteoporosis. By summarizing the specific properties of EVs and the function of EVs in both psychosocial stress and osteoporosis, respectively, it has been demonstrated that EVs are possible mediators of both, and have the prospects to be useful in innovative research areas.},
  language  = {en}
}
@misc{OseiBlockWippert2022,
  author    = {Osei, Francis and Block, Andrea and Wippert, Pia-Maria},
  title     = {Association of primary allostatic load mediators and metabolic syndrome (MetS): A systematic review},
  series = {Zweitver{\"o}ffentlichungen der Universit{\"a}t Potsdam : Gesundheitswissenschaftliche Reihe},
  journal   = {Zweitver{\"o}ffentlichungen der Universit{\"a}t Potsdam : Gesundheitswissenschaftliche Reihe},
  number    = {6},
  doi       = {10.25932/publishup-58176},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-581769},
  pages     = {16},
  year      = {2022},
  abstract  = {Allostatic load (AL) exposure may cause detrimental effects on the neuroendocrine system, leading to metabolic syndrome (MetS). The primary mediators of AL involve serum dehydroepiandrosterone sulfate (DHEAS; a functional HPA axis antagonist); further, cortisol, urinary norepinephrine (NE), and epinephrine (EPI) excretion levels (assessed within 12-h urine as a golden standard for the evaluation of the HPA axis activity and sympathetic nervous system activity). However, the evidence of an association between the primary mediators of AL and MetS is limited. This systematic review aimed to critically examine the association between the primary mediators of AL and MetS. PubMed and Web of Science were searched for articles from January 2010 to December 2021, published in English. The search strategy focused on cross-sectional and case-control studies comprising adult participants with MetS, obesity, overweight, and without chronic diseases. The STROBE checklist was used to assess study quality control. Of 770 studies, twenty-one studies with a total sample size (n = 10,666) met the eligibility criteria. Eighteen studies were cross-sectional, and three were case-control studies. The included studies had a completeness of reporting score of COR \% = 87.0 ± 6.4\%. It is to be noted, that cortisol as a primary mediator of AL showed an association with MetS in 50\% (urinary cortisol), 40\% (serum cortisol), 60\% (salivary cortisol), and 100\% (hair cortisol) of the studies. For DHEAS, it is to conclude that 60\% of the studies showed an association with MetS. In contrast, urinary EPI and urinary NE had 100\% no association with MetS. In summary, there is a tendency for the association between higher serum cortisol, salivary cortisol, urinary cortisol, hair cortisol, and lower levels of DHEAS with MetS. Future studies focusing on longitudinal data are warranted for clarification and understanding of the association between the primary mediators of AL and MetS.},
  language  = {en}
}
@article{OseiBlockWippert2022,
  author    = {Osei, Francis and Block, Andrea and Wippert, Pia-Maria},
  title     = {Association of primary allostatic load mediators and metabolic syndrome (MetS): A systematic review},
  series = {Frontiers in Endocrinology},
  volume    = {13},
  journal   = {Frontiers in Endocrinology},
  publisher = {Frontiers},
  address   = {Lausanne, Schweiz},
  issn      = {1664-2392},
  doi       = {10.3389/fendo.2022.946740},
  pages     = {16},
  year      = {2022},
  abstract  = {Allostatic load (AL) exposure may cause detrimental effects on the neuroendocrine system, leading to metabolic syndrome (MetS). The primary mediators of AL involve serum dehydroepiandrosterone sulfate (DHEAS; a functional HPA axis antagonist); further, cortisol, urinary norepinephrine (NE), and epinephrine (EPI) excretion levels (assessed within 12-h urine as a golden standard for the evaluation of the HPA axis activity and sympathetic nervous system activity). However, the evidence of an association between the primary mediators of AL and MetS is limited. This systematic review aimed to critically examine the association between the primary mediators of AL and MetS. PubMed and Web of Science were searched for articles from January 2010 to December 2021, published in English. The search strategy focused on cross-sectional and case-control studies comprising adult participants with MetS, obesity, overweight, and without chronic diseases. The STROBE checklist was used to assess study quality control. Of 770 studies, twenty-one studies with a total sample size (n = 10,666) met the eligibility criteria. Eighteen studies were cross-sectional, and three were case-control studies. The included studies had a completeness of reporting score of COR \% = 87.0 ± 6.4\%. It is to be noted, that cortisol as a primary mediator of AL showed an association with MetS in 50\% (urinary cortisol), 40\% (serum cortisol), 60\% (salivary cortisol), and 100\% (hair cortisol) of the studies. For DHEAS, it is to conclude that 60\% of the studies showed an association with MetS. In contrast, urinary EPI and urinary NE had 100\% no association with MetS. In summary, there is a tendency for the association between higher serum cortisol, salivary cortisol, urinary cortisol, hair cortisol, and lower levels of DHEAS with MetS. Future studies focusing on longitudinal data are warranted for clarification and understanding of the association between the primary mediators of AL and MetS.},
  language  = {en}
}
@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}
}
@misc{HeWuertzKozakKuehletal.2021,
  author    = {He, Yangyang and Wuertz-Kozak, Karin and Kuehl, Linn K. and Wippert, Pia-Maria},
  title     = {Extracellular vesicles: potential mediators of psychosocial stress contribution to osteoporosis?},
  series = {Postprints der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe},
  journal   = {Postprints der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe},
  number    = {11},
  issn      = {1866-8372},
  doi       = {10.25932/publishup-52300},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-523007},
  pages     = {17},
  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}
}
@misc{WippertWiebking2018,
  author    = {Wippert, Pia-Maria and Wiebking, Christine},
  title     = {Stress and Alterations in the Pain Matrix},
  series = {Postprints der Universit{\"a}t Potsdam : Humanwissenschaftliche Reihe},
  journal   = {Postprints der Universit{\"a}t Potsdam : Humanwissenschaftliche Reihe},
  number    = {438},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-412058},
  pages     = {11},
  year      = {2018},
  abstract  = {The genesis of chronic pain is explained by a biopsychosocial model. It hypothesizes an interdependency between environmental and genetic factors provoking aberrant long-term changes in biological and psychological regulatory systems. Physiological effects of psychological and physical stressors may play a crucial role in these maladaptive processes. Specifically, long-term demands on the stress response system may moderate central pain processing and influence descending serotonergic and noradrenergic signals from the brainstem, regulating nociceptive processing at the spinal level. However, the underlying mechanisms of this pathophysiological interplay still remain unclear. This paper aims to shed light on possible pathways between physical (exercise) and psychological stress and the potential neurobiological consequences in the genesis and treatment of chronic pain, highlighting evolving concepts and promising research directions in the treatment of chronic pain. Two treatment forms (exercise and mindfulness-based stress reduction as exemplary therapies), their interaction, and the dose-response will be discussed in more detail, which might pave the way to a better understanding of alterations in the pain matrix and help to develop future prevention and therapeutic concepts},
  language  = {en}
}
@article{WippertWiebking2018,
  author    = {Wippert, Pia-Maria and Wiebking, Christine},
  title     = {Stress and Alterations in the Pain Matrix},
  series = {International Journal of Environmental Research and Public Health},
  volume    = {15},
  journal   = {International Journal of Environmental Research and Public Health},
  number    = {4},
  publisher = {MDPI AG},
  address   = {Basel},
  issn      = {1660-4601},
  doi       = {10.3390/ijerph15040785},
  pages     = {1 -- 11},
  year      = {2018},
  abstract  = {The genesis of chronic pain is explained by a biopsychosocial model. It hypothesizes an interdependency between environmental and genetic factors provoking aberrant long-term changes in biological and psychological regulatory systems. Physiological effects of psychological and physical stressors may play a crucial role in these maladaptive processes. Specifically, long-term demands on the stress response system may moderate central pain processing and influence descending serotonergic and noradrenergic signals from the brainstem, regulating nociceptive processing at the spinal level. However, the underlying mechanisms of this pathophysiological interplay still remain unclear. This paper aims to shed light on possible pathways between physical (exercise) and psychological stress and the potential neurobiological consequences in the genesis and treatment of chronic pain, highlighting evolving concepts and promising research directions in the treatment of chronic pain. Two treatment forms (exercise and mindfulness-based stress reduction as exemplary therapies), their interaction, and the dose-response will be discussed in more detail, which might pave the way to a better understanding of alterations in the pain matrix and help to develop future prevention and therapeutic concepts},
  language  = {en}
}