Cellular senescence is a stress-response mechanism triggered by a plethora of sublethal extrinsic and/or intrinsic stimuli including, but not limited to, telomere maintenance defects, activated oncogenes, oxidative stress, mitochondrial dysfunction, proteostasis impairment and epigenetic modifications. Although growth arrested, senescent cells are still viable and metabolically highly-active, exhibiting a variety of phenotypical and molecular features.
The general view is that this non-proliferative status is adopted in order to prevent the propagation of damaged cells. Recently, novel methodologies allowing recognition of cellular senescence in vivo have facilitated the elucidation of the important, albeit distinct, roles that senescent cells may exert. It has, therefore, become clear that short term induction of senescence turns to be beneficial for cellular and, thus, organismal development and homeostasis, while its chronic persistence leads to detrimental effects, associated with ageing and age-related pathologies.
Available data indicates a key role of senescence in a growing list of pathologies, including cancer, fibrosis or diabetes. Interestingly, recent data suggests that post-mitotic cells including astrocytes and neurons may also attain a senescence-like phenotype, which could potentially determine susceptibility to neurodegenerative diseases. In addition, emerging evidence has also revealed a role for senescence in control of cell balance and tissue homeostasis in the context of normal physiology and development.
Results from animal models indicate that targeting cellular senescence therapeutically holds promise in preventing many aging-associated diseases, including neurodegeneration, lung fibrosis, sarcopenia or cardiovascular disease. These findings clearly bring senotherapeutic strategies to the frontline in such treatments.
In this Research Topic, we are welcoming original research articles and review articles that examine the role of cell senescence from development to aging and the link of cellular senescence to disease.
We welcome articles on the following subtopics:
1. Mechanisms of cell senescence.
2. Molecular and cellular markers of senescence.
3. Cell senescence and cancer.
4. Cell senescence and ageing.
5. Cell senescence and nervous system diseases.
6. Cell senescence and other diseases: fibrosis, diabetes, cardiovascular disease.
7. Cell senescence, plasticity and regeneration.
8. Cell senescence and development.
9. Transgenic models of senescence.
10. Senescence-based therapies.
Cellular senescence is a stress-response mechanism triggered by a plethora of sublethal extrinsic and/or intrinsic stimuli including, but not limited to, telomere maintenance defects, activated oncogenes, oxidative stress, mitochondrial dysfunction, proteostasis impairment and epigenetic modifications. Although growth arrested, senescent cells are still viable and metabolically highly-active, exhibiting a variety of phenotypical and molecular features.
The general view is that this non-proliferative status is adopted in order to prevent the propagation of damaged cells. Recently, novel methodologies allowing recognition of cellular senescence in vivo have facilitated the elucidation of the important, albeit distinct, roles that senescent cells may exert. It has, therefore, become clear that short term induction of senescence turns to be beneficial for cellular and, thus, organismal development and homeostasis, while its chronic persistence leads to detrimental effects, associated with ageing and age-related pathologies.
Available data indicates a key role of senescence in a growing list of pathologies, including cancer, fibrosis or diabetes. Interestingly, recent data suggests that post-mitotic cells including astrocytes and neurons may also attain a senescence-like phenotype, which could potentially determine susceptibility to neurodegenerative diseases. In addition, emerging evidence has also revealed a role for senescence in control of cell balance and tissue homeostasis in the context of normal physiology and development.
Results from animal models indicate that targeting cellular senescence therapeutically holds promise in preventing many aging-associated diseases, including neurodegeneration, lung fibrosis, sarcopenia or cardiovascular disease. These findings clearly bring senotherapeutic strategies to the frontline in such treatments.
In this Research Topic, we are welcoming original research articles and review articles that examine the role of cell senescence from development to aging and the link of cellular senescence to disease.
We welcome articles on the following subtopics:
1. Mechanisms of cell senescence.
2. Molecular and cellular markers of senescence.
3. Cell senescence and cancer.
4. Cell senescence and ageing.
5. Cell senescence and nervous system diseases.
6. Cell senescence and other diseases: fibrosis, diabetes, cardiovascular disease.
7. Cell senescence, plasticity and regeneration.
8. Cell senescence and development.
9. Transgenic models of senescence.
10. Senescence-based therapies.