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Thomas von Zglinicki

Thomas von Zglinicki

D-Index & Metrics

Biology and Biochemistry

D-Index
90
Citations
41082
World Ranking
2390
National Ranking
165

Overview

Thomas von Zglinicki is affiliated with Newcastle University in the United Kingdom and has an extensive publication record primarily focused on the biological mechanisms of aging and cellular senescence.

Their recent notable papers include:

  • Mitochondrial dysfunction in cell senescence and aging (2022, Journal of Clinical Investigation)
  • Whole-body senescent cell clearance alleviates age-related brain inflammation and cognitive impairment in mice (2021, Aging Cell)
  • Neutrophils induce paracrine telomere dysfunction and senescence in ROS-dependent manner (2021, The EMBO Journal)
  • Guidelines for minimal information on cellular senescence experimentation in vivo (2024, Cell)
  • Senescence in Post-Mitotic Cells: A Driver of Aging? (2020, Antioxidants and Redox Signaling)

The scientist frequently collaborates with other researchers. Their most frequent coauthors are:

  • Satomi Miwa (20 joint publications)
  • Edward Fielder (11 joint publications)
  • Evon Low (8 joint publications)
  • Diana Jurk (7 joint publications)
  • Avan Aihie Sayer (7 joint publications)

Thomas von Zglinicki has published in various academic venues, with a particular focus on:

  • bioRxiv (Cold Spring Harbor Laboratory) - 6 publications
  • Aging Cell - 4 publications
  • Journal of Investigative Dermatology - 3 publications
  • Ageing Research Reviews - 2 publications
  • Mechanisms of Ageing and Development - 2 publications

Their research spans several main fields including:

  • Medicine (50 publications)
  • Biochemistry, Genetics and Molecular Biology (26 publications)

Within these fields, the subfields explored include:

  • Physiology (25 publications)
  • Molecular Biology (17 publications)
  • Neurology (8 publications)
  • Immunology (8 publications)
  • Aging (8 publications)

The scientist's main research topics cover:

  • Telomeres, Telomerase, and Senescence (38 publications)
  • Genetics, Aging, and Longevity in Model Organisms (16 publications)
  • Skin Protection and Aging (14 publications)
  • Neuroinflammation and Neurodegeneration Mechanisms (12 publications)
  • Frailty in Older Adults (12 publications)
  • Mitochondrial Function and Pathology (10 publications)
  • Glioma Diagnosis and Treatment (8 publications)

Best Publications

  • A DNA damage checkpoint response in telomere-initiated senescence

    Fabrizio d'Adda di Fagagna;Philip M. Reaper;Lorena Clay-Farrace;Heike Fiegler

  • Oxidative stress shortens telomeres

    Thomas von Zglinicki

  • Cellular Senescence: Defining a Path Forward

    Vassilis Gorgoulis;Peter D. Adams;Andrea Alimonti;Dorothy C. Bennett

  • Fat tissue, aging, and cellular senescence

    Tamara Tchkonia;Dean E. Morbeck;Thomas Von Zglinicki;Jan Van Deursen

  • Mild Hyperoxia Shortens Telomeres and Inhibits Proliferation of Fibroblasts: A Model for Senescence?

    T von Zglinicki;G Saretzki;W Döcke;C Lotze

  • Feedback between p21 and reactive oxygen production is necessary for cell senescence

    João F Passos;Glyn Nelson;Chunfang Wang;Torsten Richter

  • Cellular senescence drives age-dependent hepatic steatosis.

    Mikolaj Ogrodnik;Satomi Miwa;Tamar Tchkonia;Dina Tiniakos;Dina Tiniakos

  • Chronic inflammation induces telomere dysfunction and accelerates ageing in mice

    Diana Jurk;Caroline Wilson;Joao F. Passos;Fiona Oakley

  • Mitochondrial dysfunction accounts for the stochastic heterogeneity in telomere-dependent senescence.

    João F Passos;Gabriele Saretzki;Gabriele Saretzki;Shaheda Ahmed;Shaheda Ahmed;Glyn Nelson

  • A senescent cell bystander effect: senescence-induced senescence.

    Glyn Nelson;James Wordsworth;Chunfang Wang;Diana Jurk

  • DNA damage response and cellular senescence in tissues of aging mice

    Chunfang Wang;Diana Jurk;Mandy Maddick;Glyn Nelson

  • Mitochondria are required for pro‐ageing features of the senescent phenotype

    Clara Correia-Melo;Clara Correia-Melo;Francisco D.M. Marques;Rhys Anderson;Graeme Hewitt

  • Accumulation of single-strand breaks is the major cause of telomere shortening in human fibroblasts.

    Thomas von Zglinicki;Rita Pilger;Nicolle Sitte

  • Targeting senescent cells alleviates obesity‐induced metabolic dysfunction

    Allyson K. Palmer;Ming Xu;Ming Xu;Yi Zhu;Tamar Pirtskhalava

  • Gender and telomere length : systematic review and meta-analysis

    Michael Gardner;David Bann;Laura Wiley;Rachel Cooper

  • Postmitotic neurons develop a p21-dependent senescence-like phenotype driven by a DNA damage response.

    Diana Jurk;Chunfang Wang;Satomi Miwa;Mandy Maddick

  • Role of oxidative stress in telomere length regulation and replicative senescence

    Thomas Von Zglinicki

  • Telomerase does not counteract telomere shortening but protects mitochondrial function under oxidative stress.

    Shaheda Ahmed;João F. Passos;Matthew J. Birket;Tina Beckmann

  • Cdkn1a deletion improves stem cell function and lifespan of mice with dysfunctional telomeres without accelerating cancer formation

    Aaheli Roy Choudhury;Zhenyu Ju;Meta W. Djojosubroto;Andrea Schienke

  • Health and disease in 85 year olds: baseline findings from the Newcastle 85+ cohort study

    Joanna Collerton;Karen Davies;Carol Jagger;Andrew Kingston

Frequent Co-Authors

Gabriele Saretzki
Gabriele Saretzki Newcastle University
João F. Passos
João F. Passos Mayo Clinic
Thomas B. L. Kirkwood
Thomas B. L. Kirkwood Newcastle University
Carol Jagger
Carol Jagger Newcastle University
Bernard Keavney
Bernard Keavney University of Manchester
Viktor I. Korolchuk
Viktor I. Korolchuk Newcastle University
Sarah E. Harris
Sarah E. Harris University of Edinburgh
Riccardo E. Marioni
Riccardo E. Marioni University of Edinburgh
Ian J. Deary
Ian J. Deary University of Edinburgh

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