Cellular Senescence in Health, Disease and Aging: Blessing or Curse?
Dear Colleagues, When Hayflick and Moorhead coined the term “cellular senescence” (CS) almost 60 years ago, this phenomenon was understood as a mechanism, usually induced by activation of the DNA-repair machinery, to prevent uncontrolled proliferation. Meanwhile, additional beneficial roles for CS h...
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| Idioma: | inglês |
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MDPI - Multidisciplinary Digital Publishing Institute
2022
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| Acesso em linha: | ONIX_20220111_9783036521756_774 |
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| description | Dear Colleagues, When Hayflick and Moorhead coined the term “cellular senescence” (CS) almost 60 years ago, this phenomenon was understood as a mechanism, usually induced by activation of the DNA-repair machinery, to prevent uncontrolled proliferation. Meanwhile, additional beneficial roles for CS have been identified, such as embryonic development and wound healing. The senescence associated secretory phenotype (SASP) activated in most senescent cells (SC) signals to the immune system “come here and remove me”. In organisms with young and functional immune systems, occurring SC are usually detected and removed. If SC remain in the tissue expressing the SASP, this will cause not just a damaging local inflammation but can also induce remodeling and regeneration of the surrounding tissue as well as spreading of senescence. Old organisms show reduced regenerative potential and immune function which leads to accumulation of SC. Accordingly, accumulation of SC was observed in tissues of aged individuals, but importantly also in the context of age-related disorders, neurodegenerative, or cardiovascular diseases and others. Because of its detrimental effect of the surrounding tissue, accumulation of SC is not just a consequence, but can rather been understood as a major driver of aging. In line with this, recent studies described that removal of SC showed beneficial effects on healthspan and lifespan. This exciting research led to the discovery of “senolytics”, drugs which can kill SC. Given the heterogeneity of cell types that show senescence-like phenotypes, including heart muscle and post-mitotic neuronal cells, further research is required to unravel the molecular background that renders a cell type vulnerable to senesce. Additionally, it will be important to understand how senescence is cell type-specifically induced and which molecules serve as drug targets to prevent senescence and its spreading, or actively kill SC. This special issue will shed light on the molecular pathways of CS and inflammaging and on possible strategies to interfere with these processes. Dr. Markus Riessland Guest Editor |
| format | Online |
| id | doab-20.500.12854ir-76942 |
| institution | Directory of Open Access Books |
| language | eng |
| publishDate | 2022 |
| publishDateRange | 2022 |
| publishDateSort | 2022 |
| publisher | MDPI - Multidisciplinary Digital Publishing Institute |
| publisherStr | MDPI - Multidisciplinary Digital Publishing Institute |
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| spelling | doab-20.500.12854ir-769422024-03-28T03:33:45Z Cellular Senescence in Health, Disease and Aging: Blessing or Curse? Riessland, Markus γH2AX Alzheimer’s disease DNA damage mild cognitive impairment senescence secreted protein acidic and rich in cysteine regeneration homeostasis cellular senescence biology of aging neurodegeneration brain geroscience senolytics tauopathy cancer stress response post-mitotic neuronal senescence amyotrophic lateral sclerosis senescence-associated secretory phenotype (SASP) cell-cycle melanoma pancreatic adenocarcinoma tumor infiltration chemotherapy resistance prostate inflammation AIM2 inflammasome POP3 n/a thema EDItEUR::G Reference, Information and Interdisciplinary subjects::GP Research and information: general thema EDItEUR::P Mathematics and Science::PS Biology, life sciences Dear Colleagues, When Hayflick and Moorhead coined the term “cellular senescence” (CS) almost 60 years ago, this phenomenon was understood as a mechanism, usually induced by activation of the DNA-repair machinery, to prevent uncontrolled proliferation. Meanwhile, additional beneficial roles for CS have been identified, such as embryonic development and wound healing. The senescence associated secretory phenotype (SASP) activated in most senescent cells (SC) signals to the immune system “come here and remove me”. In organisms with young and functional immune systems, occurring SC are usually detected and removed. If SC remain in the tissue expressing the SASP, this will cause not just a damaging local inflammation but can also induce remodeling and regeneration of the surrounding tissue as well as spreading of senescence. Old organisms show reduced regenerative potential and immune function which leads to accumulation of SC. Accordingly, accumulation of SC was observed in tissues of aged individuals, but importantly also in the context of age-related disorders, neurodegenerative, or cardiovascular diseases and others. Because of its detrimental effect of the surrounding tissue, accumulation of SC is not just a consequence, but can rather been understood as a major driver of aging. In line with this, recent studies described that removal of SC showed beneficial effects on healthspan and lifespan. This exciting research led to the discovery of “senolytics”, drugs which can kill SC. Given the heterogeneity of cell types that show senescence-like phenotypes, including heart muscle and post-mitotic neuronal cells, further research is required to unravel the molecular background that renders a cell type vulnerable to senesce. Additionally, it will be important to understand how senescence is cell type-specifically induced and which molecules serve as drug targets to prevent senescence and its spreading, or actively kill SC. This special issue will shed light on the molecular pathways of CS and inflammaging and on possible strategies to interfere with these processes. Dr. Markus Riessland Guest Editor 2022-01-11T13:47:10Z 2022-01-11T13:47:10Z 2021 book ONIX_20220111_9783036521756_774 9783036521756 9783036521763 https://directory.doabooks.org/handle/20.500.12854/76942 eng image/jpeg Attribution 4.0 International https://mdpi.com/books/pdfview/book/4533 https://mdpi.com/books/pdfview/book/4533 MDPI - Multidisciplinary Digital Publishing Institute 10.3390/books978-3-0365-2176-3 10.3390/books978-3-0365-2176-3 46cabcaa-dd94-4bfe-87b4-55023c1b36d0 9783036521756 9783036521763 112 Basel, Switzerland open access |
| spellingShingle | γH2AX Alzheimer’s disease DNA damage mild cognitive impairment senescence secreted protein acidic and rich in cysteine regeneration homeostasis cellular senescence biology of aging neurodegeneration brain geroscience senolytics tauopathy cancer stress response post-mitotic neuronal senescence amyotrophic lateral sclerosis senescence-associated secretory phenotype (SASP) cell-cycle melanoma pancreatic adenocarcinoma tumor infiltration chemotherapy resistance prostate inflammation AIM2 inflammasome POP3 n/a thema EDItEUR::G Reference, Information and Interdisciplinary subjects::GP Research and information: general thema EDItEUR::P Mathematics and Science::PS Biology, life sciences Cellular Senescence in Health, Disease and Aging: Blessing or Curse? |
| title | Cellular Senescence in Health, Disease and Aging: Blessing or Curse? |
| title_full | Cellular Senescence in Health, Disease and Aging: Blessing or Curse? |
| title_fullStr | Cellular Senescence in Health, Disease and Aging: Blessing or Curse? |
| title_full_unstemmed | Cellular Senescence in Health, Disease and Aging: Blessing or Curse? |
| title_short | Cellular Senescence in Health, Disease and Aging: Blessing or Curse? |
| title_sort | cellular senescence in health disease and aging blessing or curse |
| topic | γH2AX Alzheimer’s disease DNA damage mild cognitive impairment senescence secreted protein acidic and rich in cysteine regeneration homeostasis cellular senescence biology of aging neurodegeneration brain geroscience senolytics tauopathy cancer stress response post-mitotic neuronal senescence amyotrophic lateral sclerosis senescence-associated secretory phenotype (SASP) cell-cycle melanoma pancreatic adenocarcinoma tumor infiltration chemotherapy resistance prostate inflammation AIM2 inflammasome POP3 n/a thema EDItEUR::G Reference, Information and Interdisciplinary subjects::GP Research and information: general thema EDItEUR::P Mathematics and Science::PS Biology, life sciences |
| topic_facet | γH2AX Alzheimer’s disease DNA damage mild cognitive impairment senescence secreted protein acidic and rich in cysteine regeneration homeostasis cellular senescence biology of aging neurodegeneration brain geroscience senolytics tauopathy cancer stress response post-mitotic neuronal senescence amyotrophic lateral sclerosis senescence-associated secretory phenotype (SASP) cell-cycle melanoma pancreatic adenocarcinoma tumor infiltration chemotherapy resistance prostate inflammation AIM2 inflammasome POP3 n/a thema EDItEUR::G Reference, Information and Interdisciplinary subjects::GP Research and information: general thema EDItEUR::P Mathematics and Science::PS Biology, life sciences |
| url | ONIX_20220111_9783036521756_774 |