University of Groningen
The consequences of environmental conditions for antagonistic pleiotropic effects of cellular senescence
van Vliet, Thijmen
DOI:
10.33612/diss.156836397
IMPORTANT NOTE: You are advised to consult the publisher's version (publisher's PDF) if you wish to cite from it. Please check the document version below.
Document Version
Publisher's PDF, also known as Version of record
Publication date: 2021
Link to publication in University of Groningen/UMCG research database
Citation for published version (APA):
van Vliet, T. (2021). The consequences of environmental conditions for antagonistic pleiotropic effects of cellular senescence. University of Groningen. https://doi.org/10.33612/diss.156836397
Copyright
Other than for strictly personal use, it is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), unless the work is under an open content license (like Creative Commons).
Take-down policy
If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately and investigate your claim.
Downloaded from the University of Groningen/UMCG research database (Pure): http://www.rug.nl/research/portal. For technical reasons the number of authors shown on this cover page is limited to 10 maximum.
These propositions belong to the PhD thesis entitled The consequences of environmental conditions for antagonistic
pleiotropic effects of cellular senescence 1. The composition and the biological functions of the SASP remain highly heterogeneous and dependent on several (epi-)genetic and environmental clues. (this thesis) 2. Low oxygen conditions reduce the activation and establishment of a pro-inflammatory and pro-tumorigenic SASP without affecting other senescence-associated features, including a stable cell cycle arrest. (this thesis) 3. Physiologic hypoxia in tissues interferes with the induction of pro-inflammatory SASP factors in both mice and humans. (this thesis) 4. The expression and secretion of pro-inflammatory SASP factors is restrained under physiological hypoxia via AMPK mediated mTOR and downstream NF-kB inhibition. (this thesis) 5. Hypoxia-mimetic compounds modulate the development of various senescence-associated phenotypes in culture and in vivo. (this thesis) 6. Senescent cells stimulate a disease tissue environment by the chronic secretion of various pro-inflammatory and tissue-remodeling factors, a phenotype called Senescence-Associated Secretory Phenotype (SASP). (this thesis) 7. The reduced expression of markers of senescence in both humans and mice is an intriguing mechanism that could further explain the potential beneficial effects of CR. (this thesis) 8. The observation that senescent cells can have both beneficial and detrimental biological functions imply that different senescence subtypes exist with distinct phenotypes leading to opposing downstream effects. (this thesis) 9. Short term CR diet delays cutaneous wound healing in mice. (this thesis) 10. CR delays wound healing via the
impairment of senescent cells in wounds (this thesis).
