Joshua N Farr

Jan 17, 2025 | onlinelibrary.wiley.com | Joshua N Farr |David Monroe |Elizabeth Atkinson |Mitchell N. Froemming

1 Introduction There is now substantial pre-clinical evidence, principally from mouse models, that the clearance of senescent cells ameliorates a range of age-associated comorbidities (reviewed in Chaib, Tchkonia, and Kirkland 2022).

Nov 5, 2024 | medrxiv.org | Joshua N Farr |David Monroe |Elizabeth Atkinson |Mitchell N. Froemming

The authors have declared no competing interest. NCT04313634This work was supported by National Institutes of Health grants R21 AG065868 (J.N.F. and S.K.), P01 AG062413 (S.K., D.G.M.), R01 AG076515 (S.K., D.G.M.), R01 AG086085 (S.K., D.G.M.), Hevolution HR-GRO-23-1199144-8 (S.K., D.G.M.), and R01 DK128552 (J.N.F.). The funders played no role in the conduct or analyses of this study.

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).

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.

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.