Mitochondria are required for pro‐ageing features of the senescent phenotype-Reference-Cited by-同舟云学术

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

Published:2016-02-04 Issue:7 Volume:35 Page:724-742
ISSN:0261-4189
Container-title:The EMBO Journal
language:en
Short-container-title:EMBO J

Author:

Correia‐Melo Clara¹²,Marques Francisco DM¹,Anderson Rhys¹,Hewitt Graeme¹,Hewitt Rachael³,Cole John³,Carroll Bernadette M¹,Miwa Satomi¹,Birch Jodie¹,Merz Alina¹,Rushton Michael D¹,Charles Michelle¹,Jurk Diana¹,Tait Stephen WG³,Czapiewski Rafal¹,Greaves Laura⁴,Nelson Glyn¹,Bohlooly‐Y Mohammad⁵,Rodriguez‐Cuenca Sergio⁶,Vidal‐Puig Antonio⁶,Mann Derek⁷,Saretzki Gabriele¹,Quarato Giovanni⁸,Green Douglas R⁸,Adams Peter D³,Zglinicki Thomas¹,Korolchuk Viktor I¹,Passos João F¹

Affiliation:

1. Institute for Cell and Molecular Biosciences, Campus for Ageing and Vitality Newcastle University Institute for Ageing Newcastle University Newcastle upon Tyne UK

2. GABBA Program Abel Salazar Biomedical Sciences Institute University of Porto Porto Portugal

3. Institute of Cancer Sciences CR‐UK Beatson Institute University of Glasgow Glasgow UK

4. Wellcome Trust Centre for Mitochondrial Research Newcastle University Centre for Brain Ageing and Vitality Newcastle University Newcastle upon Tyne UK

5. Transgenic RAD, Discovery Sciences AstraZeneca Mölndal Sweden

6. Metabolic Research Laboratories Wellcome Trust‐MRC Institute of Metabolic Science Addenbrooke's Hospital University of Cambridge Cambridge UK

7. Faculty of Medical Sciences Institute of Cellular Medicine Newcastle University Newcastle upon Tyne UK

8. Department of Immunology St. Jude Children's Research Hospital Memphis TN USA

Funder

Biotechnology and Biological Sciences Research Council

Fundação para a Ciência e a Tecnologia

Universidade do Porto

Newcastle University

AstraZeneca

Publisher

EMBO

Subject

General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,Molecular Biology,General Neuroscience

Link

https://onlinelibrary.wiley.com/doi/pdf/10.15252/embj.201592862

Reference66 articles.

1. Chemokine Signaling via the CXCR2 Receptor Reinforces Senescence

2. A complex secretory program orchestrated by the inflammasome controls paracrine senescence

3. A DNA damage checkpoint response in telomere-initiated senescence

4. Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders

5. A reduction in ATP demand and mitochondrial activity with neural differentiation of human embryonic stem cells

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