Role of Altered Extracellular Signalling in Cellular Senescence

2019 ◽  
Author(s):  
Masaki Takasugi
Keyword(s):  
Cellular Senescence ◽  
Extracellular Signalling

The Role of Cellular Senescence in Werner Syndrome: Toward Therapeutic Intervention in Human Premature Aging

2007 ◽  
Vol 1100 (1) ◽  
pp. 455-469 ◽  
Author(s):  
T. DAVIS ◽  
F. S. WYLLIE ◽  
M. J. ROKICKI ◽  
M. C. BAGLEY ◽  
D. KIPLING
Keyword(s):  
Cellular Senescence ◽  
Therapeutic Intervention ◽  
Werner Syndrome ◽  
Premature Aging

scholarly journals Cellular Senescence in Liver Disease and Regeneration

2021 ◽  
Author(s):  
Sofia Ferreira-Gonzalez ◽  
Daniel Rodrigo-Torres ◽  
Victoria L. Gadd ◽  
Stuart J. Forbes
Keyword(s):  
Cell Cycle ◽  
Liver Disease ◽  
Cell Cycle Arrest ◽  
Genomic Instability ◽  
Cellular Senescence ◽  
Cell Populations ◽  
Cycle Arrest ◽  
Relevant Role ◽  
Extent Of Damage

AbstractCellular senescence is an irreversible cell cycle arrest implemented by the cell as a result of stressful insults. Characterized by phenotypic alterations, including secretome changes and genomic instability, senescence is capable of exerting both detrimental and beneficial processes. Accumulating evidence has shown that cellular senescence plays a relevant role in the occurrence and development of liver disease, as a mechanism to contain damage and promote regeneration, but also characterizing the onset and correlating with the extent of damage. The evidence of senescent mechanisms acting on the cell populations of the liver will be described including the role of markers to detect cellular senescence. Overall, this review intends to summarize the role of senescence in liver homeostasis, injury, disease, and regeneration.

The role of cellular senescence in cardiac disease: basic biology and clinical relevance

2021 ◽  
Author(s):  
Mozhdeh Mehdizadeh ◽  
Martin Aguilar ◽  
Eric Thorin ◽  
Gerardo Ferbeyre ◽  
Stanley Nattel
Keyword(s):  
Cellular Senescence ◽  
Cardiac Disease ◽  
Clinical Relevance ◽  
Basic Biology

Traumatic stress and cellular senescence: The role of war-captivity and homecoming stressors in later life telomere length

2018 ◽  
Vol 238 ◽  
pp. 129-135 ◽  
Author(s):  
Jacob Y. Stein ◽  
Yafit Levin ◽  
Orit Uziel ◽  
Heba Abumock ◽  
Zahava Solomon
Keyword(s):  
Telomere Length ◽  
Cellular Senescence ◽  
Traumatic Stress ◽  
Later Life

scholarly journals Role of Age-Related Mitochondrial Dysfunction in Sarcopenia

2020 ◽  
Vol 21 (15) ◽  
pp. 5236 ◽  
Author(s):  
Evelyn Ferri ◽  
Emanuele Marzetti ◽  
Riccardo Calvani ◽  
Anna Picca ◽  
Matteo Cesari ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cellular Senescence ◽  
Significant Loss ◽  
Muscle Aging ◽  
Age Related ◽  
Mitochondrial Functions ◽  
Health Quality ◽  
Skeletal Muscle Aging ◽  
And Function

Skeletal muscle aging is associated with a significant loss of skeletal muscle strength and power (i.e., dynapenia), muscle mass and quality of life, a phenomenon known as sarcopenia. This condition affects nearly one-third of the older population and is one of the main factors leading to negative health outcomes in geriatric patients. Notwithstanding the exact mechanisms responsible for sarcopenia are not fully understood, mitochondria have emerged as one of the central regulators of sarcopenia. In fact, there is a wide consensus on the assumption that the loss of mitochondrial integrity in myocytes is the main factor leading to muscle degeneration. Mitochondria are also key players in senescence. It has been largely proven that the modulation of mitochondrial functions can induce the death of senescent cells and that removal of senescent cells improves musculoskeletal health, quality, and function. In this review, the crosstalk among mitochondria, cellular senescence, and sarcopenia will be discussed with the aim to elucidate the role that the musculoskeletal cellular senescence may play in the onset of sarcopenia through the mediation of mitochondria.

Targeting cancer's Achilles’ heel: role of BCL-2 inhibitors in cellular senescence and apoptosis

2019 ◽  
Vol 11 (17) ◽  
pp. 2287-2312 ◽  
Author(s):  
Aarti Anantram ◽  
Mariam Degani
Keyword(s):  
Nuclear Magnetic Resonance ◽  
Magnetic Resonance ◽  
Tumor Growth ◽  
Cellular Senescence ◽  
Anticancer Agents ◽  
Anticancer Therapy ◽  
Targeted Chemotherapy ◽  
Structure Based Drug Design ◽  
Selective Targeting

Members of the antiapoptotic BCL-2 proteins are involved in tumor growth, progression and survival, and are also responsible for chemoresistance to conventional anticancer agents. Early efforts to target these proteins yielded some active compounds; however, newer methodologies involving structure-based drug design, Nuclear Magnetic Resonance (NMR)-based screening and fragment-based screening yielded more potent compounds. Discovery of specific as well as nonspecific inhibitors of this class of proteins has resulted in great advances in targeted chemotherapy and decrease in chemoresistance. Here, we review the history and current progress in direct as well as selective targeting of the BCL-2 proteins for anticancer therapy.

scholarly journals Role of histone deacetylase 2 in epigenetics and cellular senescence: implications in lung inflammaging and COPD

2012 ◽  
Vol 303 (7) ◽  
pp. L557-L566 ◽  
Author(s):  
Hongwei Yao ◽  
Irfan Rahman
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Histone Deacetylase ◽  
Dna Damage Response ◽  
Cellular Senescence ◽  
Premature Aging ◽  
Epigenetic Mechanism ◽  
Histone Deacetylase 2 ◽  
Damage Response

Histone deacetylase 2 (HDAC2) is a class I histone deacetylase that regulates various cellular processes, such as cell cycle, senescence, proliferation, differentiation, development, apoptosis, and glucocorticoid function in inhibiting inflammatory response. HDAC2 has been shown to protect against DNA damage response and cellular senescence/premature aging via an epigenetic mechanism in response to oxidative stress. These phenomena are observed in patients with chronic obstructive pulmonary disease (COPD). HDAC2 is posttranslationally modified by oxidative/carbonyl stress imposed by cigarette smoke and oxidants, leading to its reduction via an ubiquitination-proteasome dependent degradation in lungs of patients with COPD. In this perspective, we have discussed the role of HDAC2 posttranslational modifications and its role in regulation of inflammation, histone/DNA epigenetic modifications, DNA damage response, and cellular senescence, particularly in inflammaging, and during the development of COPD. We have also discussed the potential directions for future translational research avenues in modulating lung inflammaging and cellular senescence based on epigenetic chromatin modifications in diseases associated with increased oxidative stress.

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