Authors
Christina D Camell, Matthew J Yousefzadeh, Yi Zhu, Larissa GP Langhi Prata, Matthew A Huggins, Mark Pierson, Lei Zhang, Ryan D O’Kelly, Tamar Pirtskhalava, Pengcheng Xun, Keisuke Ejima, Ailing Xue, Utkarsh Tripathi, Jair Machado Espindola-Netto, Nino Giorgadze, Elizabeth J Atkinson, Christina L Inman, Kurt O Johnson, Stephanie H Cholensky, Timothy W Carlson, Nathan K LeBrasseur, Sundeep Khosla, M Gerard O’Sullivan, David B Allison, Stephen C Jameson, Alexander Meves, Ming Li, YS Prakash, Sergio E Chiarella, Sara E Hamilton, Tamara Tchkonia, Laura J Niedernhofer, James L Kirkland, Paul D Robbins
Publication date
2021/6/8
Journal
Science
Publisher
American Association for the Advancement of Science
Description
INTRODUCTION
The COVID-19 pandemic revealed enhanced vulnerability of the elderly and chronically ill to adverse outcomes upon severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Senescence is a cell fate elicited by cellular stress that results in changes in gene expression, morphology, metabolism, and resistance to apoptosis. Senescent cells (SnCs) secrete pro-inflammatory factors, called the senescence-associated secretory phenotype (SASP). SnCs accumulate with age and drive chronic inflammation. In human cells and tissues and using a new infection paradigm, we asked whether SnCs are a cause of adverse outcomes of infection with aging. This is relevant because SnCs can be selectively eliminated in vivo with a new class of therapeutics called senolytics, potentially affording a new approach to treat COVID-19.
RATIONALE
We hypothesized that SnCs, because of their …
Total citations
Scholar articles
CD Camell, MJ Yousefzadeh, Y Zhu, LGPL Prata… - Science, 2021