Anthropology Notes On – Senescence – For W.B.C.S. Examination.

নৃ তত্ব নোট – বার্ধক্য – WBCS পরীক্ষা।

Aging is the major risk factor for cancer, cardiovascular disease, diabetes, and neurodegenerative disorders. Although we are far from understanding the biological basis of aging, research suggests that targeting the aging process itself could ameliorate many age-related pathologies. Senescence is a cellular response characterized by a stable growth arrest and other phenotypic alterations that include a proinflammatory secretome.Continue Reading Anthropology Notes On – Senescence – For W.B.C.S. Examination.

Senescence plays roles in normal development, maintains tissue homeostasis, and limits tumor progression. However, senescence has also been implicated as a major cause of age-related disease. In this regard, recent experimental evidence has shown that the genetic or pharmacological ablation of senescent cells extends life span and improves health span. Here, we review the cellular and molecular links between cellular senescence and aging and discuss the novel therapeutic avenues that this connection opens.

Senescence also influences the integrative aging hallmarks. Somatic multipotent stem cells facilitate tissue homeostasis; for example, hematopoietic stem cells (HSCs) renew the blood system. Stem cell exhaustion occurs with age, and the consequent decline in stem cell functionality and their capacity for renewal leads to tissue deterioration. For example, HSCs display a decreased success rate of transplantation when isolated from elderly patients (Kollman et al., 2001). This decline correlates with increased numbers of senescent HSCs (Chang et al., 2016) and diminished immunity (Geiger and Van Zant, 2002), decreased numbers of naive B and T cells (Min et al., 2005), and reduced natural killer cell activity (Mocchegiani and Malavolta, 2004). Somatic stem cell decline is not limited to high-turnover tissues. Neural stem cells (NSCs) experience reduced functionality, with limited neurogenesis capacity with age. This is marked by a twofold reduction in NSC numbers and a decreased proliferation, which correlates with increased expression of senescence markers in the regions where NSCs reside (Molofsky et al., 2006). Mesenchymal stem cells (Raggi and Berardi, 2012) and their descendants, satellite cells (Shefer et al., 2006; Lavasani et al., 2012; Sousa-Victor et al., 2014), chondrocytes (Loeser, 2009), adipocytes (Tchkonia et al., 2010), and osteoclasts (Chung et al., 2014), also display a reduced ability to self-renew with age that correlates with increased levels of senescence markers. This may have an impact in age-associated pathologies such as sarcopenia, cachexia, osteoporosis, and osteoarthritis (Fried et al., 2001).

Senescence is cellular program that induces a stable growth arrest accompanied by distinct phenotypic alterations, including chromatin remodeling, metabolic reprogramming, increased autophagy, and the implementation of a complex proinflammatory secretome (Kuilman et al., 2010; Salama et al., 2014). These complex changes to the cell largely serve to implement various aspects of senescence such as growth arrest and the senescence secretome. Despite the many facets of senescence, stable growth arrest is its defining characteristic. A permanent arrest is effective to ensure that damaged or transformed cells do not perpetuate their genomes. This growth arrest is implemented by the activation of p16^INK4a/Rb and p53/p21^CIP1 tumor suppressor networks.

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