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Introduction to Cancer, Conventional Therapies, and Bionano-Based Advanced Anticancer Strategies
Published in D. Sakthi Kumar, Aswathy Ravindran Girija, Bionanotechnology in Cancer, 2023
Cellular stress that activates P53 induces apoptosis. During the cell cycle arrest, the weak and sustained activation can promote cell death known as senescence. Cellular senescence is pathophysiological condition by which the cells permanently lose their proliferative capacity. Senescence cell shows specific-morphological features, including flattening, nuclear enlargement, enriched with vacuoles, and altered chromatin structure. In the biochemical level, cellular senescence is characterized by increased ß-galactocidase activity that increases senescence markers, such as P15, P16, P21, P53, and ARF.
Cell death after irradiation: How, when and why cells die
Published in Michael C. Joiner, Albert J. van der Kogel, Basic Clinical Radiobiology, 2018
Cellular senescence is the term given to the observation that over time normal cells permanently lose their ability to divide. These cells remain present, metabolically intact and may or may not display functional changes. Senescence was first described by Leonard Hayflick in 1965 in cultured primary cells that exhibit an initial period of exponential growth, followed by a permanent arrest termed replicative senescence or the Hayflick limit (9). Replicative senescence is associated with the aging process and correlates with the gradual shortening of telomeres at the ends of chromosomes during the exponential growth period.
Chronic obstructive pulmonary disease
Published in Louis-Philippe Boulet, Applied Respiratory Pathophysiology, 2017
Julie Milot, Mathieu Morissette
Cellular senescence occurs when oxidative stress induces damage too severe to allow for efficient repair but not severe enough to lead to cell death. A senescent cell has high levels of p16 and B-galactosidase activity. These cells are still metabolically active but can no longer contribute to tissue regeneration. If cellular damage cannot be efficiently repaired, the cell will engage apoptotic pathways involving the transcription factor p53 as well as pro-apoptotic mitochondrial factors Bax, PUMA, and NOXA. These elements will lead the cell toward apoptosis, a “clean” type of cell death with restricted amount of alarmins being released. If cellular damage is very severe, the cell will not have the capacity to engage apoptotic pathways and will become necrotic, releasing alarmins that will trigger and/or amplify the inflammatory response [52,54,55].
Novel therapeutic approaches in the management of chronic kidney disease: a narrative review
Published in Postgraduate Medicine, 2023
Panagiotis Theofilis, Aikaterini Vordoni, Rigas G. Kalaitzidis
Other agents have been explored in kidney diseases. B-cell activating factor (BAFF) may be implicated in the development of kidney dysfunction since it raises the expression of profibrotic factors through the tumor necrosis factor receptor‑associated factor 6 (TRAF6)/NF‑κB signaling pathway [49]. In patients with IgA nephropathy, increased BAFF levels are associated with disease severity [49]. At the same time, in vivo inhibition of BAFF could ameliorate the induced kidney injury [49]. A Proliferation Inducing Ligand (APRIL) inhibitors may also be of use in the treatment of IgA nephropathy, as they were proven effective and safe in a recent experimental study [50]. Additionally, therapies targeting cellular senescence in CKD (senolytics, senomorphics, rejuvenating agents) are another promising prospect that ought to be further investigated in future studies [51].
The epidemiologic and biologic basis for classifying older age as a high-risk, immunocompromising condition for pneumococcal vaccine policy
Published in Expert Review of Vaccines, 2021
Lindsay R. Grant, Mary P. E. Slack, Qi Yan, Krzysztof Trzciński, Jane Barratt, Elizabeth Sobczyk, James Appleby, Alejandro Cané, Luis Jodar, Raul E. Isturiz, Bradford D. Gessner
Two hallmark characteristics of immunosenescence are cellular senescence and inflammaging. Cellular senescence is the metabolically altered state of cells that leads to cessation of cell division and cell clearance [54]. Senescent cells secrete pro-inflammatory molecules resulting in a low-grade chronic and systemic inflammatory state, termed inflammaging, which occurs in the absence of detectable infection [55]. As aging, cellular senescence, and inflammaging have different effects on different cell-types, identification of age-related changes in the innate and adaptive immune systems that might contribute to an increased susceptibility to infection is challenging. The evidence for a specific effect on pneumococcal infection is even more limited, and largely based on pneumococcal specific models in older mice [53] (Supplemental Table 4 [55–88]). Here, we summarize current knowledge about the impact of aging, cellular senescence, and inflammaging on host susceptibility to pneumococcal infection.
Genistein alleviates H2O2-induced senescence of human umbilical vein endothelial cells via regulating the TXNIP/NLRP3 axis
Published in Pharmaceutical Biology, 2021
Guihua Wu, Siming Li, Guangjin Qu, Jiajia Hua, Jing Zong, Xiaofeng Li, Fanghui Xu
Senescence is an irreversible form of long-term cell-cycle arrest, caused by excessive intracellular or extracellular stress or damage (Noren Hooten and Evans 2017; Dodig et al. 2019), and cellular senescence refers to the arrest in the G1 phase of the cell-cycle (Vicencio et al. 2008). In addition, cellular senescence has been reported to be a potent anti-cancer mechanism that arrests the proliferation of mitotically competent cells to prevent malignant transformation (Chinta et al. 2015). Researchers have identified many stressors that are able to induce senescence, such as H2O2 (Song et al. 2014). Li et al. (2016) proposed that H2O2 treatment significantly inhibited the migration and proliferation of HUVECs in a dose-dependent manner. In our study, in order to establish a primary cell-induced disease model that was more clinically and physiologically relevant to human disease, H2O2-treated HUVECs were employed to discover the possible small molecules or the underlying mechanism for improving H2O2-induced senescence of HUVECs. Besides, it was noted that H2O2 inhibited the proliferation and cell cycle G1/S transition and promoted the senescence of HUVECs.