About Cellular Senescence in Stress and Aging
Cellular Senescence in Stress and Aging
About this Collection
This collection is now closed to submissions.
Cells are constantly under various types of stress that push them away from their balance point. In this respect, cell fate depends upon its ability to deal with, respond and overcome any stressful condition that jeopardize its integrity, through the activation of stress response mechanisms. Cellular senescence is such a stress response mechanism that involves replicative arrest, apoptosis resistance, epigenetic alterations, chromatin rearrangement, metabolic deregulation and a complex pro-inflammatory secretory phenotype.
Cellular senescence was first considered to be a process for preventing the proliferation of abnormal cells, e.g. cancer cells. However, during the last decades it has become apparent that this unique biological phenomenon exceeds far beyond cessation of cell division and tumour suppression. In fact, cellular senescence exerts a hormetic/ bimodal effect; acute induction of cellular senescence plays beneficial role in cellular and tissue homeostasis, whereas chronic accumulation of senescent cells conversely leads to tissue dysfunction. Accordingly, cellular senescence has been implicated in aging and age-related pathologies, such as neurodegenerative or cardiovascular diseases.
The biology of cellular senescence represents an emerging area of interest. Of great importance, similarly to mitotic cells it has been suggested that post-mitotic cells are also capable of undergoing senescence. In both mitotic and post-mitotic cells, cellular senescence can be triggered by various exogenous and endogenous stimuli, including but not limited to telomere dysfunction, DNA damage, overexpression of oncogenes, oxidative stress, chemotherapeutics, epigenetic modifiers, perturbed proteostasis, or – lastly included – viruses. Intriguingly, entering the senescent state is not a “one-way ticket for cells”, since under specific circumstances escape from senescence is also an option, as supported by recent findings.
As signalling pathways and molecular mechanisms that govern cellular senescence are being revealed, novel strategies for preventing and treating age-related diseases are devised, based on a new class of drugs that target senescent cells; this is the dawn of the era of senotherapeutics.
This collection invites articles in the field of cellular senescence, not only as a hallmark of aging but also as a stress response mechanism implicated in circumstances that cellular and tissue homeostasis in impaired. We especially invite material focusing on the following issues:
This collection is now closed.
This collection is part of the Cell & Molecular Biology Gateway.
Any questions about this collection? Please get in contact directly with research@f1000.com.
Cells are constantly under various types of stress that push them away from their balance point. In this respect, cell fate depends upon its ability to deal with, respond and overcome any stressful condition that jeopardize its integrity, through the activation of stress response mechanisms. Cellular senescence is such a stress response mechanism that involves replicative arrest, apoptosis resistance, epigenetic alterations, chromatin rearrangement, metabolic deregulation and a complex pro-inflammatory secretory phenotype.
Cellular senescence was first considered to be a process for preventing the proliferation of abnormal cells, e.g. cancer cells. However, during the last decades it has become apparent that this unique biological phenomenon exceeds far beyond cessation of cell division and tumour suppression. In fact, cellular senescence exerts a hormetic/ bimodal effect; acute induction of cellular senescence plays beneficial role in cellular and tissue homeostasis, whereas chronic accumulation of senescent cells conversely leads to tissue dysfunction. Accordingly, cellular senescence has been implicated in aging and age-related pathologies, such as neurodegenerative or cardiovascular diseases.
The biology of cellular senescence represents an emerging area of interest. Of great importance, similarly to mitotic cells it has been suggested that post-mitotic cells are also capable of undergoing senescence. In both mitotic and post-mitotic cells, cellular senescence can be triggered by various exogenous and endogenous stimuli, including but not limited to telomere dysfunction, DNA damage, overexpression of oncogenes, oxidative stress, chemotherapeutics, epigenetic modifiers, perturbed proteostasis, or – lastly included – viruses. Intriguingly, entering the senescent state is not a “one-way ticket for cells”, since under specific circumstances escape from senescence is also an option, as supported by recent findings.
As signalling pathways and molecular mechanisms that govern cellular senescence are being revealed, novel strategies for preventing and treating age-related diseases are devised, based on a new class of drugs that target senescent cells; this is the dawn of the era of senotherapeutics.
This collection invites articles in the field of cellular senescence, not only as a hallmark of aging but also as a stress response mechanism implicated in circumstances that cellular and tissue homeostasis in impaired. We especially invite material focusing on the following issues:
- Metabolic pathways implicated in cellular senescence
- The interplay between autophagy and cellular senescence
- Immuno-senescence
- The role of cellular senescence in aging
- Cellular senescence in clinical / pathological entities
- Senotherapeutics: a new player in clinical practice
This collection is now closed.
This collection is part of the Cell & Molecular Biology Gateway.
Any questions about this collection? Please get in contact directly with research@f1000.com.
Collection Advisors
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Vassilis V. Gorgoulis
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Panagiotis V.S. Vasileiou
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Muthuswamy Balasubramanyam
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