Cellular Senescence: Difference between revisions

Cellular Senescence (view source)

Revision as of 17:36, 9 January 2024

402 bytes removed , 9 January

no edit summary

VisualWikitext

Strimo

Bureaucrats, Administrators

2,851

edits

Revision as of 17:34, 9 January 2024 (view source) Strimo (talk \| contribs) m (Strimo moved page Senescent Cells to Cellular Senescence) ← Older edit		Revision as of 17:36, 9 January 2024 (view source) Strimo (talk \| contribs) No edit summary Tag: Visual edit Newer edit →
Line 1:		Line 1:
	[[File:~~DALL·E 2023~~-~~10-15 05.28.43~~ - ~~Photo of senescent cells magnified under a microscope, showing their characteristic enlarged and flattened morphology. The cells are stained with a bl~~.png\|right\|frameless\|Photo of senescent cells magnified under a microscope, showing their characteristic enlarged and flattened morphology. The cells are stained with a blue dye, highlighting the irregular nucleus and presence of senescence-associated β-galactosidase.]]		[[File:cellular-senescence-process.png\|right\|frameless]]
	'''Cellular senescence''', a state in which cells lose their ability to divide and function properly, is a pivotal concept in the study of aging and longevity. This phenomenon is intricately linked with the Hayflick limit, named after biologist Leonard Hayflick, who discovered in the 1960s that most somatic cells have a limited capacity to divide, typically around 40 to 60 times, before they enter senescence. The limitation arises primarily due to telomere shortening—the protective ends of chromosomes that diminish with each cellular division. Once telomeres reach a critical length, the cell perceives it as DNA damage, prompting cell cycle arrest and thereby preventing potential genetic instability.		'''Cellular senescence''', a state in which cells lose their ability to divide and function properly, is a pivotal concept in the study of aging and longevity. This phenomenon is intricately linked with the Hayflick limit, named after biologist Leonard Hayflick, who discovered in the 1960s that most somatic cells have a limited capacity to divide, typically around 40 to 60 times, before they enter senescence. The limitation arises primarily due to telomere shortening—the protective ends of chromosomes that diminish with each cellular division. Once telomeres reach a critical length, the cell perceives it as DNA damage, prompting cell cycle arrest and thereby preventing potential genetic instability.