L
Laura J. Niedernhofer
Researcher at University of Minnesota
Publications - 199
Citations - 18051
Laura J. Niedernhofer is an academic researcher from University of Minnesota. The author has contributed to research in topics: DNA repair & Senescence. The author has an hindex of 55, co-authored 173 publications receiving 12983 citations. Previous affiliations of Laura J. Niedernhofer include Sapienza University of Rome & Scripps Health.
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Journal ArticleDOI
The Achilles’ heel of senescent cells: from transcriptome to senolytic drugs
Yi-Yi Zhu,Tamara Tchkonia,Tamar Pirtskhalava,Adam C. Gower,Husheng Ding,Nino Giorgadze,Allyson K. Palmer,Yuji Ikeno,Yuji Ikeno,Gene B. Hubbard,Gene B. Hubbard,Marc E. Lenburg,Steven P. O'Hara,Nicholas F. LaRusso,Jordan D. Miller,Carolyn M Roos,Grace C Verzosa,Nathan K. LeBrasseur,Jonathan D. Wren,Joshua N. Farr,Sundeep Khosla,Michael B. Stout,Sara J. McGowan,Heike Fuhrmann-Stroissnigg,Aditi U. Gurkar,Jing-jing Zhao,Debora Colangelo,Akaitz Dorronsoro,Yuan Yuan Ling,Amira S. Barghouthy,Diana C. Navarro,Tokio Sano,Paul D. Robbins,Laura J. Niedernhofer,James L. Kirkland +34 more
TL;DR: The results demonstrate the feasibility of selectively ablating senescent cells and the efficacy of senolytics for alleviating symptoms of frailty and extending healthspan.
Journal ArticleDOI
Cellular Senescence: Defining a Path Forward
Vassilis G. Gorgoulis,Peter D. Adams,Andrea Alimonti,Dorothy C. Bennett,Oliver Bischof,Cleo L. Bishop,Judith Campisi,Manuel Collado,Konstantinos Evangelou,Gerardo Ferbeyre,Jesús Gil,Eiji Hara,Valery Krizhanovsky,Diana Jurk,Andrea B. Maier,Masashi Narita,Laura J. Niedernhofer,João F. Passos,Paul D. Robbins,Clemens A. Schmitt,John M. Sedivy,Konstantinos Vougas,Thomas von Zglinicki,Daohong Zhou,Manuel Serrano,Marco Demaria +25 more
TL;DR: A consensus from the International Cell Senescence Association (ICSA) is presented, defining and discussing key cellular and molecular features of senescence and offering recommendations on how to use them as biomarkers.
Journal ArticleDOI
Senolytics improve physical function and increase lifespan in old age
Ming Xu,Ming Xu,Tamar Pirtskhalava,Joshua N. Farr,Bettina M. Weigand,Bettina M. Weigand,Allyson K. Palmer,Megan M. Weivoda,Christina L. Inman,Mikolaj Ogrodnik,Mikolaj Ogrodnik,Christine M Hachfeld,Daniel G. Fraser,Jennifer L Onken,Kurt O. Johnson,Grace C Verzosa,Larissa G.P. Langhi,Moritz Weigl,Nino Giorgadze,Nathan K. LeBrasseur,Jordan D. Miller,Diana Jurk,Ravinder J. Singh,David B. Allison,David B. Allison,Keisuke Ejima,Keisuke Ejima,Gene B. Hubbard,Yuji Ikeno,Yuji Ikeno,Hajrunisa Cubro,Vesna D. Garovic,Xiaonan Hou,S. John Weroha,Paul D. Robbins,Laura J. Niedernhofer,Sundeep Khosla,Tamara Tchkonia,James L. Kirkland +38 more
TL;DR: It is demonstrated that transplanting relatively small numbers of senescent cells into young mice is sufficient to cause persistent physical dysfunction, as well as to spread cellular senescence to host tissues, and a senolytic can reverse this dysfunction and potently increase lifespan in aged mice.
Journal ArticleDOI
Identification of a novel senolytic agent, navitoclax, targeting the Bcl-2 family of anti-apoptotic factors.
Yi Zhu,Tamara Tchkonia,Heike Fuhrmann-Stroissnigg,Haiming Dai,Yuanyuan Y. Ling,Michael B. Stout,Tamar Pirtskhalava,Nino Giorgadze,Kurt O. Johnson,Cory B. Giles,Jonathan D. Wren,Laura J. Niedernhofer,Paul D. Robbins,James L. Kirkland +13 more
TL;DR: The hypothesis‐driven, bioinformatics‐based approach used to discover that dasatinib (D) and quercetin (Q) are senolytic can be extended to increase the repertoire ofsenolytic drugs, including additional cell type‐specific senolytics agents.
Journal ArticleDOI
A new progeroid syndrome reveals that genotoxic stress suppresses the somatotroph axis
Laura J. Niedernhofer,George A. Garinis,Anja Raams,Astrid S. Lalai,Andria Rasile Robinson,Esther Appeldoorn,Hanny Odijk,Roos Oostendorp,Anwaar Ahmad,Wibeke J. Van Leeuwen,Arjan F. Theil,Wim Vermeulen,Gijsbertus T. J. van der Horst,Peter Meinecke,Wim J. Kleijer,Jan Vijg,Nicolaas G. J. Jaspers,Jan H.J. Hoeijmakers +17 more
TL;DR: It is concluded that unrepaired cytotoxic DNA damage induces a highly conserved metabolic response mediated by the IGF1/insulin pathway, which re-allocates resources from growth to somatic preservation and life extension, and demonstrates that ageing and end-of-life fitness are determined both by stochastic damage and genetics.