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  1. Book ; Thesis: Langfristige endokrinologische Auswirkungen mittelschwerer und schwerer Schädel-Hirn-Traumata im Kindes- und Jugendalter

    Materne, Marie Malene / Hübner, Angela / Hofbauer, Lorenz C.

    2021  

    Institution Klinik und Poliklinik für Kinder- und Jugendmedizin
    Author's details von Marie Malente Materne aus Richterswil ; Klinik und Poliklinik für Kinder- und Jugendmedizin [Dresden]
    Subject code 618.92 ; 610
    Language German
    Size VII, 143 Blätter, Illustrationen, Diagramme
    Publishing place Dresden
    Publishing country Germany
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Dissertation, Technische Universität Dresden, Medizinische Fakultät, 2021
    HBZ-ID HT030595025
    Database Catalogue ZB MED Medicine, Health

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    2023 E 1379 order for loan Magazin

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  2. Article ; Online: Denosumab - protection for bone and beyond?

    Hofbauer, Lorenz C / Rauner, Martina

    The Journal of clinical endocrinology and metabolism

    2024  

    Language English
    Publishing date 2024-03-29
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 3029-6
    ISSN 1945-7197 ; 0021-972X
    ISSN (online) 1945-7197
    ISSN 0021-972X
    DOI 10.1210/clinem/dgae207
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  3. Article ; Online: Deconstructing cellular senescence in bone and beyond.

    Hofbauer, Lorenz C / Lademann, Franziska / Rauner, Martina

    The Journal of clinical investigation

    2023  Volume 133, Issue 8

    Abstract: Osteocytes are specialized bone cells that orchestrate skeletal remodeling. Senescent osteocytes are characterized by an activation of cyclin-dependent kinase inhibitor p16Ink4a and have been implicated in the pathogenesis of several bone loss disorders. ...

    Abstract Osteocytes are specialized bone cells that orchestrate skeletal remodeling. Senescent osteocytes are characterized by an activation of cyclin-dependent kinase inhibitor p16Ink4a and have been implicated in the pathogenesis of several bone loss disorders. In this issue of the JCI, Farr et al. have now shown that systemic removal of senescent cells (termed senolysis) prevented age-related bone loss at the spine and femur and mitigated bone marrow adiposity through a robust effect on osteoblasts and osteoclasts, whereas cell-specific senolysis in osteocytes alone was only partially effective. Surprisingly, transplantation of senescent fibroblasts into the peritoneum of young mice caused host osteocyte senescence associated with bone loss. This refined concept of osteocyte senescence and the effects of remote senolysis may help to develop improved senolytic strategies against multisystem aging in bone and beyond.
    MeSH term(s) Mice ; Animals ; Cellular Senescence/physiology ; Bone and Bones ; Aging/pathology ; Osteoblasts ; Osteoclasts ; Osteocytes ; Bone Diseases, Metabolic
    Language English
    Publishing date 2023-04-17
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI169069
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  4. Article ; Online: Deconstructing cellular senescence in bone and beyond

    Lorenz C. Hofbauer / Franziska Lademann / Martina Rauner

    The Journal of Clinical Investigation, Vol 133, Iss

    2023  Volume 8

    Abstract: Osteocytes are specialized bone cells that orchestrate skeletal remodeling. Senescent osteocytes are characterized by an activation of cyclin-dependent kinase inhibitor p16Ink4a and have been implicated in the pathogenesis of several bone loss disorders. ...

    Abstract Osteocytes are specialized bone cells that orchestrate skeletal remodeling. Senescent osteocytes are characterized by an activation of cyclin-dependent kinase inhibitor p16Ink4a and have been implicated in the pathogenesis of several bone loss disorders. In this issue of the JCI, Farr et al. have now shown that systemic removal of senescent cells (termed senolysis) prevented age-related bone loss at the spine and femur and mitigated bone marrow adiposity through a robust effect on osteoblasts and osteoclasts, whereas cell-specific senolysis in osteocytes alone was only partially effective. Surprisingly, transplantation of senescent fibroblasts into the peritoneum of young mice caused host osteocyte senescence associated with bone loss. This refined concept of osteocyte senescence and the effects of remote senolysis may help to develop improved senolytic strategies against multisystem aging in bone and beyond.
    Keywords Medicine ; R
    Language English
    Publishing date 2023-04-01T00:00:00Z
    Publisher American Society for Clinical Investigation
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Reduced Bone Regeneration in Rats With Type 2 Diabetes Mellitus as a Result of Impaired Stromal Cell and Osteoblast Function-A Computer Modeling Study.

    Jaber, Mahdi / Hofbauer, Lorenz C / Hofbauer, Christine / Duda, Georg N / Checa, Sara

    JBMR plus

    2023  Volume 7, Issue 11, Page(s) e10809

    Abstract: Bone has the fascinating ability to self-regenerate. However, under certain conditions, such as type 2 diabetes mellitus (T2DM), this ability is impaired. T2DM is a chronic metabolic disease known by the presence of elevated blood glucose levels that is ... ...

    Abstract Bone has the fascinating ability to self-regenerate. However, under certain conditions, such as type 2 diabetes mellitus (T2DM), this ability is impaired. T2DM is a chronic metabolic disease known by the presence of elevated blood glucose levels that is associated with reduced bone regeneration capability, high fracture risk, and eventual non-union risk after a fracture. Several mechanical and biological factors relevant to bone regeneration have been shown to be affected in a diabetic environment. However, whether impaired bone regeneration in T2DM can be explained due to mechanical or biological alterations remains unknown. To elucidate the relevance of either one, the aim of this study was to investigate the relative contribution of T2DM-related alterations on either cellular activity or mechanical stimuli driving bone regeneration. A previously validated in silico computer modeling approach that was capable of explaining bone regeneration in uneventful conditions of healing was further developed to investigate bone regeneration in T2DM. Aspects analyzed included the presence of mesenchymal stromal cells (MSCs), cellular migration, proliferation, differentiation, apoptosis, and cellular mechanosensitivity. To further verify the computer model findings against in vivo data, an experimental setup was replicated, in which regeneration was compared in healthy and diabetic after a rat femur bone osteotomy stabilized with plate fixation. We found that mechanical alterations had little effect on the reduced bone regeneration in T2DM and that alterations in MSC proliferation, MSC migration, and osteoblast differentiation had the highest effect. In silico predictions of regenerated bone in T2DM matched qualitatively and quantitatively those from ex vivo μCT at 12 weeks post-surgery when reduced cellular activities reported in previous in vitro and in vivo studies were included in the model. The presented findings here could have clinical implications in the treatment of bone fractures in patients with T2DM. © 2023 The Authors.
    Language English
    Publishing date 2023-10-02
    Publishing country England
    Document type Journal Article
    ISSN 2473-4039
    ISSN (online) 2473-4039
    DOI 10.1002/jbm4.10809
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  6. Article ; Online: MiR-144-5p and miR-21-5p do not drive bone disease in a mouse model of type 1 diabetes mellitus.

    Daamouch, Souad / Blüher, Matthias / Vázquez, David Carro / Hackl, Matthias / Hofbauer, Lorenz C / Rauner, Martina

    JBMR plus

    2024  Volume 8, Issue 5, Page(s) ziae036

    Abstract: The increased risk of fractures in patients with type 1 diabetes mellitus (T1DM) is nowadays well recognized. However, the exact mechanism of action of diabetic bone disease has not been fully elucidated. MicroRNAs (miRNAs) are gene regulators that ... ...

    Abstract The increased risk of fractures in patients with type 1 diabetes mellitus (T1DM) is nowadays well recognized. However, the exact mechanism of action of diabetic bone disease has not been fully elucidated. MicroRNAs (miRNAs) are gene regulators that operate post-transcriptionally and have been implicated in the development of various metabolic disorders including T1DM. Previous studies have implicated a role for miR-144-5p and miR-21-5p, which are involved in controlling oxidative stress by targeting Nrf2, in T1DM. To date, it is unclear whether miR-144-5p and miR-21-5p affect bone health in T1DM. Thus, this study aimed to investigate the influence of miR-144-5p and miR-21-5p knockdown in the development of bone disease in T1DM male mice. Therefore, T1DM was induced in 10-wk-old male mice using streptozotocin (STZ). One week later, after development of hyperglycemia, antagomir-144-5p and antagomir-21-5p or their non-targeting control were administered at 10 mg/kg BW once a week until the end of the experiment. At 14 wk of age, glucose levels, bone, and fat mass were analyzed. The results revealed that treating T1DM male mice with antagomir-144-5p and antagomir-21-5p did not protect against diabetes development or bone loss, despite the successful downregulation of the miRNAs and the normalization of Nrf2 mRNA levels in bone tissue. Histological and serological parameters of bone formation or resorption were not altered by the antagomir treatment. Finally, we measured the expression of miRNA-144-5p or miRNA-21-5p in the serum of 30 individuals with T1DM and compared them to non-diabetic controls, but did not find an altered expression of either miRNA. In conclusion, the knockdown of miR-144-5p and miR-21-5p does not affect STZ-induced diabetes development or loss of bone mass in male mice. However, it does normalize expression of the anti-oxidant factor Nrf2 in diabetic bone tissue.
    Language English
    Publishing date 2024-04-06
    Publishing country England
    Document type Journal Article
    ISSN 2473-4039
    ISSN (online) 2473-4039
    DOI 10.1093/jbmrpl/ziae036
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  7. Article ; Online: Thyroid hormone receptor Thra and Thrb knockout differentially affects osteoblast biology and thyroid hormone responsiveness in vitro.

    Lademann, Franziska / Tsourdi, Elena / Hofbauer, Lorenz C / Rauner, Martina

    Journal of cellular biochemistry

    2023  Volume 124, Issue 12, Page(s) 1948–1960

    Abstract: Thyroid hormones (TH) are important modulators of bone remodeling and thus, thyroid diseases, in particular hyperthyroidism, are able to compromise bone quality and fracture resistance. TH actions on bone are mediated by the thyroid hormone receptors (TR) ...

    Abstract Thyroid hormones (TH) are important modulators of bone remodeling and thus, thyroid diseases, in particular hyperthyroidism, are able to compromise bone quality and fracture resistance. TH actions on bone are mediated by the thyroid hormone receptors (TR) TRα1 and TRβ1, encoded by Thra and Thrb, respectively. Skeletal phenotypes of mice lacking Thra (Thra
    MeSH term(s) Mice ; Animals ; Receptors, Thyroid Hormone/genetics ; Receptors, Thyroid Hormone/metabolism ; Thyroid Hormone Receptors alpha/genetics ; Thyroid Hormone Receptors alpha/metabolism ; Thyroid Hormones/metabolism ; Thyroid Hormone Receptors beta/genetics ; Thyroid Hormone Receptors beta/metabolism ; Osteoblasts/metabolism ; Osteoclasts/metabolism ; Biology ; RANK Ligand/metabolism ; Mice, Knockout
    Chemical Substances Receptors, Thyroid Hormone ; Thyroid Hormone Receptors alpha ; Thyroid Hormones ; Thyroid Hormone Receptors beta ; RANK Ligand
    Language English
    Publishing date 2023-11-22
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 392402-6
    ISSN 1097-4644 ; 0730-2312
    ISSN (online) 1097-4644
    ISSN 0730-2312
    DOI 10.1002/jcb.30500
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  8. Article ; Online: [No title information]

    Jaschke, Nikolai P / Rachner, Tilman D / Hofbauer, Lorenz C

    Deutsche medizinische Wochenschrift (1946)

    2021  Volume 146, Issue 15, Page(s) 1017

    Title translation Erwiderung auf den Leserbrief zum Beitrag: „Testosteronmangel im Alter – was ist zu tun“.
    MeSH term(s) Humans ; Testosterone
    Chemical Substances Testosterone (3XMK78S47O)
    Language German
    Publishing date 2021-05-19
    Publishing country Germany
    Document type Letter ; Comment
    ZDB-ID 200446-x
    ISSN 1439-4413 ; 0012-0472
    ISSN (online) 1439-4413
    ISSN 0012-0472
    DOI 10.1055/a-1423-2691
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  9. Article ; Online: The Impact of COVID-19 in Bone Metabolism: Basic and Clinical Aspects.

    Tsourdi, Elena / Hofbauer, Lorenz C / Rauner, Martina

    Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme

    2022  Volume 54, Issue 8, Page(s) 540–548

    Abstract: The use of standard procedures for the diagnosis of osteoporosis and assessment of fracture risk significantly decreased during the COVID-19 pandemic, while the incidence of fragility fractures was mostly unaltered. Both COVID-19 per se and its ... ...

    Abstract The use of standard procedures for the diagnosis of osteoporosis and assessment of fracture risk significantly decreased during the COVID-19 pandemic, while the incidence of fragility fractures was mostly unaltered. Both COVID-19 per se and its treatments are associated with a negative impact on bone health. Preclinical models show that mice infected with SARS-CoV2 even without symptoms display loss of trabecular bone mass two weeks post infection, due to increased numbers of osteoclasts. Osteoporosis medications do not aggravate the clinical course of COVID-19, while preclinical data suggests possible beneficial effects of some therapies. While vitamin D deficiency is clearly associated with a worse clinical course of COVID-19, evidence of improved patient outcome with vitamin D supplementation is lacking. Osteoporosis treatment should not be generally discontinued, and recommendations for substituting therapies are available. Osteoporosis therapies do not interfere with the efficacy or side-effect profiles of COVID-19 vaccines and should not be stopped or indefinitely delayed because of vaccination.
    MeSH term(s) Animals ; COVID-19 ; COVID-19 Vaccines ; Fractures, Bone/complications ; Humans ; Mice ; Osteoporosis/drug therapy ; Pandemics ; RNA, Viral/therapeutic use ; SARS-CoV-2 ; Vitamin D/therapeutic use
    Chemical Substances COVID-19 Vaccines ; RNA, Viral ; Vitamin D (1406-16-2)
    Language English
    Publishing date 2022-04-13
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 80125-2
    ISSN 1439-4286 ; 0018-5043
    ISSN (online) 1439-4286
    ISSN 0018-5043
    DOI 10.1055/a-1825-9641
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  10. Article ; Online: Transferrin receptor 2 mitigates periodontitis-driven alveolar bone loss.

    Lösser, Lennart / Ledesma-Colunga, Maria G / Andrés Sastre, Enrique / Scholtysek, Carina / Hofbauer, Lorenz C / Noack, Barbara / Baschant, Ulrike / Rauner, Martina

    Journal of cellular physiology

    2024  Volume 239, Issue 2, Page(s) e31172

    Abstract: Periodontitis is associated with significant alveolar bone loss. Patients with iron overload suffer more frequently from periodontitis, however, the underlying mechanisms remain largely elusive. Here, we investigated the role of transferrin receptor 2 ( ... ...

    Abstract Periodontitis is associated with significant alveolar bone loss. Patients with iron overload suffer more frequently from periodontitis, however, the underlying mechanisms remain largely elusive. Here, we investigated the role of transferrin receptor 2 (Tfr2), one of the main regulators of iron homeostasis, in the pathogenesis of periodontitis and the dental phenotype under basal conditions in mice. As Tfr2 suppresses osteoclastogenesis, we hypothesized that deficiency of Tfr2 may exacerbate periodontitis-induced bone loss. Mice lacking Tfr2 (Tfr2
    MeSH term(s) Animals ; Humans ; Mice ; Alveolar Bone Loss/genetics ; Alveolar Bone Loss/metabolism ; Iron ; Osteoclasts ; Periodontitis/genetics ; Periodontitis/metabolism ; Receptors, Transferrin/genetics ; X-Ray Microtomography ; Mice, Inbred C57BL ; Cells, Cultured
    Chemical Substances Iron (E1UOL152H7) ; Receptors, Transferrin ; TRF2 protein, mouse
    Language English
    Publishing date 2024-01-12
    Publishing country United States
    Document type Journal Article
    ZDB-ID 3116-1
    ISSN 1097-4652 ; 0021-9541
    ISSN (online) 1097-4652
    ISSN 0021-9541
    DOI 10.1002/jcp.31172
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