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Jul 2, 2024 | 
nature.com | Joshua N Farr |Jad G. Sfeir |Dominik Saul |Kai Yu |Tamara Tchkonia |Nathan K. LeBrasseur | +2 more
AbstractPreclinical evidence demonstrates that senescent cells accumulate with aging and that senolytics delay multiple age-related morbidities, including bone loss. Thus, we conducted a phase 2 randomized controlled trial of intermittent administration of the senolytic combination dasatinib plus quercetin (D + Q) in postmenopausal women (n = 60 participants).
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May 16, 2024 | 
jci.org | Dominik Saul |Madison L. Doolittle |Jennifer L. Rowsey |Mitchell N. Froemming
ResearchAgingBone biologyOpen Access | 10.1172/JCI179834 J Clin Invest. https://doi.org/10.1172/JCI179834. Copyright © 2024, Saul et al. This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
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Feb 7, 2024 | 
biorxiv.org | Dominik Saul |Madison L. Doolittle |Jennifer L. Rowsey |Mitchell N. Froemming
AbstractCells expressing features of senescence, including upregulation of p21 and p16, appear transiently following tissue injury, yet the properties of these cells or how they contrast with age-induced senescent cells remains unclear. Here, we used skeletal injury as a model and identified the rapid appearance following fracture of p21+ cells expressing senescence markers, mainly as osteochondroprogenitors (OCHs) and neutrophils.
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Jan 2, 2024 | 
nature.com | Stella G. Victorelli |James Chapman |Joel Riley |Diana Jurk |Lilian Sales Gomez |Joshua N Farr | +11 more
Correction to: Nature https://doi.org/10.1038/s41586-023-06621-4 Published online 11 October 2023In the version of this article initially published, US NIH grants R33AG61456-4 and R01AG064165 were missing from the Acknowledgements section and have now been inserted in the HTML and PDF versions of the article.
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Oct 11, 2023 | 
nature.com | Stella G. Victorelli |James Chapman |Joel Riley |Diana Jurk |Lilian Sales Gomez |Joshua N Farr | +11 more
AbstractSenescent cells drive age-related tissue dysfunction partially through the induction of a chronic senescence-associated secretory phenotype (SASP)1. Mitochondria are major regulators of the SASP; however, the underlying mechanisms have not been elucidated2. Mitochondria are often essential for apoptosis, a cell fate distinct from cellular senescence. During apoptosis, widespread mitochondrial outer membrane permeabilization (MOMP) commits a cell to die3.
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Jul 31, 2023 | 
nature.com | Madison L. Doolittle |Dominik Saul |Kevin D Pavelko |Joshua N Farr |David Monroe
Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
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May 7, 2023 | 
aging-us.com | Parinya Samakkarnthai |Dominik Saul |Lei Zhang |Zaira Aversa
Discussion In the present study, we used multiple, complementary approaches to evaluate the possible effects of zoledronic acid on cellular senescence.
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May 7, 2023 | 
aging-us.com | Parinya Samakkarnthai |Dominik Saul |Lei Zhang |Zaira Aversa
Research Paper Volume 15, Issue 9 pp 3331—3355 1 Division of Endocrinology, Mayo Clinic, Rochester, MN 55905, USA 2 Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN 55905, USA 3 Division of Endocrinology, Phramongkutklao Hospital and College of Medicine, Bangkok 10400, Thailand 4 Department of Trauma and Reconstructive Surgery, Eberhard Karls University Tübingen, BG Trauma Center Tübingen, Tübingen 72076, Germany 5 Institute on the Biology of Aging and Metabolism,...
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Apr 17, 2023 | 
jci.org | Joshua N Farr |Dominik Saul |Madison L. Doolittle |Japneet Kaur
AbstractClearance of senescent cells (SnCs) can prevent several age-related pathologies, including bone loss. However, the local versus systemic roles of SnCs in mediating tissue dysfunction remain unclear. Thus, we developed a mouse model (p16-LOX-ATTAC) that allowed for inducible SnC elimination (senolysis) in a cell-specific manner and compared the effects of local versus systemic senolysis during aging using bone as a prototype tissue.
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Feb 24, 2023 | 
biorxiv.org | Parinya Samakkarnthai |Dominik Saul |Lei Zhang |Zaira Aversa
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