Senescence: Difference between revisions

Content deleted Content added
Citation bot (talk | contribs)
Removed proxy/dead URL that duplicated identifier. Removed access-date with no URL. Removed parameters. | Use this bot. Report bugs. | Suggested by Headbomb | Category:CS1 maint: PMC embargo expired | #UCB_Category 6/18
m task, replaced: journal=NPJ → journal=npj
Line 49:
 
{{Excerpt|Stem cell theory of aging|Other theories of aging}}
 
=== Evolutionary aging theories ===
{{Main|Evolution of ageing}}
Line 78 ⟶ 79:
 
====Chemical damage====
{{Section tooVery long section|date=March 2023}}
[[Image:Edward S. Curtis Collection People 086.jpg|thumb|200px|Elderly [[Klamath people|Klamath]] woman photographed by [[Edward S. Curtis]] in 1924]]{{See also|DNA damage theory of aging}}
One of the earliest aging theories was the ''[[Rate-of-living theory|Rate of Living Hypothesis]]'' described by [[Raymond Pearl]] in 1928<ref>{{Cite book| vauthors = Pearl R |title=The Rate of Living, Being an Account of Some Experimental Studies on the Biology of Life Duration|publisher=Alfred A. Knopf|year=1928|location=New York}}{{Page needed|date=September 2010}}</ref> (based on earlier work by [[Max Rubner]]), which states that fast [[basal metabolic rate]] corresponds to short [[maximum life span]].
Line 91 ⟶ 92:
[[Reactive oxygen species|Free radicals]] can damage proteins, [[lipid]]s or [[DNA damage theory of aging|DNA]]. [[Glycation]] mainly damages proteins. Damaged proteins and lipids accumulate in [[lysosome]]s as [[lipofuscin]]. Chemical damage to structural proteins can lead to loss of function; for example, damage to [[collagen]] of [[blood vessel]] walls can lead to vessel-wall stiffness and, thus, [[hypertension]], and vessel wall thickening and reactive tissue formation ([[atherosclerosis]]); similar processes in the [[kidney]] can lead to [[kidney failure]]. Damage to [[enzyme]]s reduces cellular functionality. Lipid [[redox|peroxidation]] of the inner [[mitochondrial membrane]] reduces the [[electric potential]] and the ability to generate energy. It is probably no accident that nearly all of the so-called "[[accelerated aging disease]]s" are due to defective [[DNA repair]] enzymes.<ref name="KimuraSuzuki2008">{{cite book| vauthors = Bernstein H, Payne CM, Bernstein C, Garewal H, Dvorak K |url={{google books |plainurl=y |id=arjZMwAACAAJ|page=1}}|title=New Research on DNA Damage|publisher=Nova Science Publishers|year=2008|isbn=978-1604565812| veditors = Kimura H, Suzuki A |pages=1–47 |chapter= Cancer and aging as consequences of un-repaired DNA damage. |chapter-url=https://www.novapublishers.com/catalog/product_info.php?products_id=43247 }}</ref><ref name="pmid27164092">{{cite journal | vauthors = Pan MR, Li K, Lin SY, Hung WC | title = Connecting the Dots: From DNA Damage and Repair to Aging | journal = International Journal of Molecular Sciences | volume = 17 | issue = 5 | pages = 685 | date = May 2016 | pmid = 27164092 | pmc = 4881511 | doi = 10.3390/ijms17050685 | doi-access = free }}</ref>
 
[[DNA damage (naturally occurring)|DNA damage]] was proposed in a 2021 review to be the underlying cause of aging because of the mechanistic link of DNA damage to nearly every aspect of the aging phenotype.<ref name = Schumacher2021>Schumacher B, Pothof J, Vijg J, Hoeijmakers JHJ. The central role of DNA damage in the ageing process. Nature. 2021 Apr;592(7856):695-703. doi: 10.1038/s41586-021-03307-7. Epub 2021 Apr 28. PMID: 33911272; PMCID: PMC9844150</ref> DNA damage-induced [[epigenetics|epigenetic]] alterations, such as [[DNA methylation]] and many [[histone]] modifications, appear to be of particular importance to the aging process.<ref name = Schumacher2021/> Evidence for the theory that DNA damage is the fundamental cause of aging was first reviewed in 1981.<ref>Gensler HL, Bernstein H. DNA damage as the primary cause of aging. Q Rev Biol. 1981 Sep;56(3):279-303. doi: 10.1086/412317. PMID: 7031747</ref>
 
It is believed that the [[impact of alcohol on aging]] can be partly explained by alcohol's activation of the [[HPA axis]], which stimulates [[glucocorticoid]] secretion, long-term exposure to which produces symptoms of aging.<ref>{{cite journal | vauthors = Spencer RL, Hutchison KE | title = Alcohol, aging, and the stress response | journal = Alcohol Research & Health | volume = 23 | issue = 4 | pages = 272–83 | year = 1999 | pmid = 10890824 | pmc = 6760387 | url = http://pubs.niaaa.nih.gov/publications/arh23-4/272-283.pdf }}</ref>
Line 149 ⟶ 150:
 
== Healthspans and aging in society ==
[[File:Global aging demographics.webp|thumb|Past and projected age of the human world population through time as of 2021<ref name="10.1038/s41536-021-00169-5">{{cite journal |last1=Garmany |first1=Armin |last2=Yamada |first2=Satsuki |last3=Terzic |first3=Andre |title=Longevity leap: mind the healthspan gap |journal=NPJnpj Regenerative Medicine |date=23 September 2021 |volume=6 |issue=1 |page=57 |doi=10.1038/s41536-021-00169-5 |pmid=34556664 |pmc=8460831 |language=en |issn=2057-3995|doi-access=free}}
* Non-profit hospital press release: {{cite news |first1=Susan |last1=Buckles |title=A regenerative reset for aging » Center for Regenerative Biotherapeutics |url=https://regenerativemedicineblog.mayoclinic.org/2021/10/07/a-regenerative-reset-for-aging |access-date=1 March 2023 |work=[[Mayo Clinic]]}}</ref>]]
[[File:Healthspan-lifespan gap.webp|thumb|Healthspan-lifespan gap (LHG)<ref name="10.1038/s41536-021-00169-5"/>]]
Line 160 ⟶ 161:
== Interventions ==
{{Excerpt|Life extension}}{{Further|Life extension}}
 
==See also==
{{div col|colwidth=22em}}