Survival Pathways and Stress Tolerance Mechanisms in Senescence Programs
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".
Deadline for manuscript submissions: closed (30 November 2020) | Viewed by 5420
Special Issue Editor
Interests: ER stress; Unfolded Protein Response; Senescence; Cancer; Signaling pathways
Special Issue Information
Dear Colleagues,
Senescence is a complex cellular state, which can be viewed as a stress response phenotype. Various mechanisms can induce senescence, including telomere shortening, oxidative stress and damage to macromolecules, exposure to chemotherapeutic drugs, and the activation of oncogenes such as Ras. Despite a robust cell cycle arrest, senescent cells have been shown to promote both beneficial and detrimental effects through cell autonomous and non-cell autonomous mechanisms. It is now well established that an increase in senescent cells is causally implicated in generating age-related phenotypes, including metabolic, neurodegenerative diseases, impaired wound healing, and fibrosis. Regarding cancer, evidence has shown that senescent cells can escape from senescence programs to re-enter the cell cycle and promote tumor progression. A fundamental question that remains is understanding why and how a cell acquires and maintains a senescent phenotype. This Special Issue, entitled Survival Pathways and Stress Tolerance Mechanisms in Senescence Programs, is devoted to gaining a better understanding of the mechanisms/pathways that contribute to the establishment and maintaining of the senescent phenotype. Original articles or reviews are welcome.
Dr. Olivier Pluquet
Guest Editor
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Keywords
- Signal transduction
- Senescence-associated secretory phenotype
- Senescence features (epigenetic regulation, DNA damage pathway, etc.)
- Cell cycle
- Resistance to apoptosis
- Oxidative stress
- Metabolism (lipids, proteins, synthesis, and degradation)
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