China
Africa
Explore chapters and articles related to this topic
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.
Muscle Pain and Aging
Published in Robert M. Bennett, The Clinical Neurobiology of Fibromyalgia and Myofascial Pain, 2020
From what has been synthetically reported, it is evident that the problem of pain, particularly muscle pain, in the elderly represents the challenge of the future for the pain clinician and researcher, the challenge of relieving the burden on an increasing portion of the general population. Since senescence represents a disease per se, every possible effort should be made to eliminate or decrease at least the algogenic component that so often accompanies old age.
Notes on Genetic and Radiation Control of Senescence
Published in Nate F. Cardarelli, The Thymus in Health and Senescence, 2019
Senescence arises from either the repression of specific genes that prevent the associated characteristics, or from the derepression of certain genes that, once free to act, cause the symptomatology of aging. At the genome level, no other mechanism of senescence control has been postulated. The various aging theories considered earlier that have any potential for explaining underlying mechanisms reduce to an inescapable absolute: somewhere gene(s) are switched on or off. Consequently, many scientists have searched for the switching device.
Baicalein attenuates bleomycin-induced lung fibroblast senescence and lung fibrosis through restoration of Sirt3 expression
Published in Pharmaceutical Biology, 2023
Yuan Ji-hong, Ma Yu, Yuan Ling-hong, Gong Jing-jing, Xu Ling-li, Wang Lv, Jin Yong-mei
Cell senescence refers to a relatively stable state in which cells irreversibly leave the cell cycle and lose their proliferative ability under the action of signal transduction. In recent decades, cell senescence has attracted widespread attention as it increases the morbidity of fibroproliferative pulmonary diseases in elderly individuals (Parimon et al. 2021). Recent studies have demonstrated that epithelial progenitor cell dysfunction and cellular senescence, including epithelial and fibroblast senescence, were associated with the pathological development of IPF (Demaria et al. 2014; Lehmann et al. 2017). Hohmann et al. (2019) found that quercetin could attenuate BLM-induced lung fibrosis and injury by inhibiting fibroblast senescence and enhancing FasL- or TRAIL-induced apoptosis. Of note, Cui et al. (2018) demonstrated that baicalein could mitigate TGF-β1-mediated lung FMT differentiation through the inhibition of miR-21 expression. In the present study, it was found that baicalein reversed BLM-induced lung fibroblast senescence and increased the transcript levels of proinflammatory and profibrotic SASP factors in mice. However, whether baicalein enhances lung fibroblast apoptosis in BLM-treated mice and regulates the expression of miR-21 is worthy of further study.
Identifying the challenges for successful pharmacotherapeutic management of sarcopenia
Published in Expert Opinion on Pharmacotherapy, 2022
In addition to non-steroidal anti-inflammatory drugs (NSAIDs) to target inflammatory cytokine signaling, mTOR inhibitors, renin–angiotensin system modulators, and metformin, are being investigated to address age-related metabolic dysfunction with relevance to sarcopenia [11]. Mimicking the benefits of exercise has therapeutic potential for sarcopenia and many other muscle disorders, especially when patients are unable (or limited in their capacity) to perform any physical activity. Attention has focussed on targeting AMP-activated protein kinase (AMPK) signaling to elicit (endurance-like) benefits to skeletal muscle, with several compounds being repurposed as ‘exercise mimetics’ [12]. Mimicking the benefits of resistance training (and possibly co-treating with more selective AMPK activators), must also be considered if these approaches are to be effective pharmacotherapies for sarcopenia. Senolytic drugs (‘senotherapeutics’) that target senescent cells or inhibit the senescence-associated secretory phenotype, have received considerable attention for their potential application to treat age-related diseases [13].
Correlation between Keratoconus and Pollution
Published in Ophthalmic Epidemiology, 2021
Tristan Jurkiewicz, Anne-Sophie Marty
Most studies only quantify cell death but do not take into account changes in cell function. Senescence can lead to a reduction in a tissue’s ability to perform its function.46–48 We have seen that particles’ action on healthy corneas. However, patients’ cornea with keratoconus could be particularly sensitive to the accumulation of reactive oxygen species and that process could be favoured by a dysfunction of antioxidant mechanisms.30 In the long term, the pollution could increase the rate of cell death and cause a degradation process of the extracellular matrix leading to corneal thinning.49 The impacts of particles on the structure of the stroma and the accumulation of reactive oxygen species could be greater than in healthy corneas. This could induce the development of keratoconus in genetically susceptible individuals and aggravate its evolution when already present.