Editing Senescence (section)

==Definition and characteristics==
''Organismal senescence'' is the aging of whole organisms. Actuarial senescence can be defined as an increase in mortality or a decrease in [[fecundity]] with age. The [[Gompertz–Makeham law of mortality]] says that the age-dependent component of the [[mortality rate]] [[exponential growth|increases exponentially]] with age.

[[Aging]] is characterized by the declining ability to respond to stress, increased [[homeostasis|homeostatic]] imbalance, and increased risk of [[aging-associated diseases]] including [[cancer]] and [[heart disease]]. Aging has been defined as "a progressive deterioration of physiological function, an intrinsic age-related process of loss of viability and increase in vulnerability."<ref>{{Cite web |title=Aging and Gerontology Glossary |url=http://www.senescence.info/glossary.html |access-date=26 February 2011 |archive-date=19 October 2019 |archive-url=https://web.archive.org/web/20191019200702/http://www.senescence.info/glossary.html |url-status=live }}</ref>

In 2013, a group of scientists defined nine [[hallmarks of aging]] that are common between organisms with emphasis on mammals:
* [[genomic instability]],
* [[telomere]] attrition,
* [[epigenetic]] alterations,
* loss of [[proteostasis]],
* deregulated [[nutrient sensing]],
* mitochondrial dysfunction,
* cellular senescence,
* stem cell exhaustion,
* altered intercellular communication<ref name="pmid23746838">{{cite journal | vauthors = López-Otín C, Blasco MA, Partridge L, Serrano M, Kroemer G | title = The hallmarks of aging | journal = Cell | volume = 153 | issue = 6 | pages = 1194–217 | date = June 2013 | pmid = 23746838 | pmc = 3836174 | doi = 10.1016/j.cell.2013.05.039 }}</ref>

In a decadal update, three hallmarks have been added, totaling 12 proposed hallmarks: 
* disabled [[macroautophagy]]
* [[chronic inflammation]]
* [[dysbiosis]]<ref name="10.1016/j.cell.2022.11.001">{{cite journal |last1=López-Otín |first1=Carlos |last2=Blasco |first2=Maria A. |last3=Partridge |first3=Linda |last4=Serrano |first4=Manuel |last5=Kroemer |first5=Guido |title=Hallmarks of aging: An expanding universe |journal=Cell |date=19 January 2023 |volume=186 |issue=2 |pages=243–278 |doi=10.1016/j.cell.2022.11.001 |pmid=36599349 |s2cid=255394876 |language=English |doi-access=free }}</ref>

The environment induces damage at various levels, e.g. [[DNA damage theory of aging|damage to DNA]], and damage to tissues and cells by oxygen [[radical (chemistry)|radicals]] (widely known as [[Free-radical theory|free radicals]]), and some of this damage is not repaired and thus accumulates with time.<ref name="pmid1383772">{{cite journal |vauthors=Holmes GE, Bernstein C, Bernstein H |title=Oxidative and other DNA damages as the basis of aging: a review |journal=Mutat. Res. |volume=275 |issue=3–6 |pages=305–15 |date=September 1992 |pmid=1383772 |doi= 10.1016/0921-8734(92)90034-m}}</ref> [[Cloning]] from [[somatic cell]]s rather than germ cells may begin life with a higher initial load of damage. [[Dolly the sheep]] died young from a contagious lung disease, but data on an entire population of cloned individuals would be necessary to measure mortality rates and quantify aging.{{citation needed|date=December 2019}}

The evolutionary theorist George Williams wrote, "It is remarkable that after a seemingly miraculous feat of [[morphogenesis]], a complex [[metazoa]]n should be unable to perform the much simpler task of merely maintaining what is already formed."<ref name = "Williams_1957">{{cite journal | vauthors = Williams GC | year = 1957 | title = Pleiotropy, natural selection, and the evolution of senescence | journal = Evolution | volume = 11 | issue = 4| pages = 398–411 | doi = 10.2307/2406060 | jstor = 2406060 }}</ref>