Understanding the odd science of aging.

By Thomas B. L. Kirkwood. Cell, 2005

1,954 citations recorded by the source corpus.

Subfields: Aging, Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/145fa94d3e50fe215193f4f6542139d5b5879e01

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Aging

In Genetics

In Molecular Biology

Citations in the corpus

Fasting Cycles Retard Growth of Tumors and Sensitize a Range of Cancer Cell Types to Chemotherapy (2012, background): “Fasting apparently protects normal cells by reallocating energy toward maintenance pathways from reproduction and growth processes when nutrients are scarce or absent (2, 10, 13, 15).”
The evolutionary ecology of senescence (2008, neutral): “There is some empirical evidence in support of each (Kirkwood & Austad 2000) and Wilson et al (2008) provide a short review of the testing of these hypotheses.”
Stem cells, ageing and the quest for immortality (2006, background): “Two theories have emerged that integrate the possibility of genetic programmes that direct the ageing process with the notion that such programmes are not likely to have arisen by pressures of natural selectio”
Nonequilibrium physics in biology (2019, background): “…process of continuous decay of physiological functions, which even- 46 tually leads to death, but experiments on model organisms show that ageing can be significantly delayed by suitable genetic manipulations and in appropriate environments (Gems and L., 2013; Kenyon, 2010; Kirkwood, 2005).”
Education and Cognitive Functioning Across the Life Span (2020, background): “…reasons include the possibility that individual differences in change arise from random processes or from processes that are themselves difficult to measure or are rarely measured—for example, human senescence may have an inherently random component (Kirkwood, 2005; Raz & Daugherty, 2018).”
Oxidative Stress Resistance in Deinococcus radiodurans (2011, background): “Empirical evidence from diverse lines of research suggests that aging is a process of a gradual increase in somatic mutations leading eventually to frailty and an increased risk of a spectrum of age-associated diseases (300, 301).”
An integrated view of oxidative stress in aging: basic mechanisms, functional effects, and pathological considerations. (2007, background): “In fact, while many investigators focus on a limited number of genes in selected model organisms, current evidence has led to the suggestion that it is impossible for aging to be accounted for by a single theory (127).”
DNA damage and its links to neurodegeneration (2014, background): “…and the Evolution of Senescence, George C. Williams (1957) observed, “It is remarkable that after a seemingly miraculous feat of morphogenesis a complex metazoan should be unable to perform the much simpler task of merely maintaining what is already formed” (Kirkwood, 2005; Williams, 1957).”
Mitochondrial Dysfunction Accounts for the Stochastic Heterogeneity in Telomere-Dependent Senescence (2007, neutral): “causes age-related frailty, disease, and death [1].”
Telomere dysfunction induces metabolic and mitochondrial compromise (2011, neutral): “Finally, anti-p53 chromatin-immunoprecipitation assays in G2 Terc−/− p53+/+, but not G2 Terc−/− p53−/−, MEFs demonstrated physical binding between p53 and (1) PGC-1α fragments containing p53 binding elements at −564 and −954, but not −2317, and (2) PGC1β fragments containing p53 binding elements at ”
Aging, frailty and age-related diseases (2010, background): “Aging can be conceptualized as a process of accumulation of deficits, taking place in different individuals in different ways, with a variety of rates for different organ systems, depending on the interplay of intrinsic and extrinsic factors (Mitnitski et al. 2001; Kirkwood 2005).”
A new progeroid syndrome reveals that genotoxic stress suppresses the somatotroph axis (2006, background): “Gene ontology classification (Supplementary Table 4) revealed: (1) global attenuation of the somatotroph, lactotroph and thyrotroph hormonal axes and other growth-promoting mechanisms; (2) downregulation of oxidative and carbohydrate metabolism; (3) upregulation of genes associated with glycogen syn”
Role of advanced glycation end products in cellular signaling (2014, neutral): “…. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 412 Receptors for advanced glycation end products—structure and function. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 414 Receptor for AGEs…”