Hayflick, his limit, and cellular ageing

Shay, Jerry W.; Wright, Woodring E.

doi:10.1038/35036093

Cited by 764Telomeres, Telomerase, and SenescenceGenetics, Aging, and Longevity in Model OrganismsMicrotubule and mitosis dynamics

Hayflick, his limit, and cellular ageing

Shay, Jerry W., Wright, Woodring E.·2000·Nature Reviews Molecular Cell Biology

DOI 10.1038/35036093

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Abstract

Almost 40 years ago, Leonard Hayflick discovered that cultured normal human cells have limited capacity to divide, after which they become senescent -- a phenomenon now known as the 'Hayflick limit'. Hayflick's findings were strongly challenged at the time, and continue to be questioned in a few circles, but his achievements have enabled others to make considerable progress towards understanding and manipulating the molecular mechanisms of ageing.

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Finite cell lines undergo a programmed process of biological 'ageing' and eventually cease replication and enter a state of senescence.
“Finite cell lines are cultures of cells that can be sub-cultured many times but undergo a programmed process of biological 'ageing' (Campisi and di Fagagna, 2007) and eventually cease replication and enter a state of senescence (Shay and Wright, 2000; Swim and Parker, 1957).”
From Guidance document on Good cell and tissue culture practice 2.0 (GCCP 2.0) (2021) · cites this paper as Shay and Wright, 2000
Proliferating cells reach the Hayflick limit largely because repeated DNA replication in the absence of telomerase causes telomeres to progressively shorten and eventually malfunction.
“Over the ensuing decades, it was discovered that proliferating cells reach the so-called Hayflick limit largely because repeated DNA replication in the absence of telomerase causes telomeres to progressively shorten and eventually malfunction (Shay and Wright, 2000).”
From Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors (2005) · cites this paper as Shay and Wright, 2000

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The Coming of Age of WI-381 1This work was not supported in whole or in part by Grant R01 AG 03478 from the National Institute on Aging, NIH, Bethesda, Md.2 2A version of this paper was presented at the thirty-fourth annual meeting of the Tissue Culture Association, at the Session-in-Depth, “Origin of Cell Lines,” organized and chaired by Dr. Robert E. Stevenson, Orlando, Florida, 13 June 1983. This was an invited paper in which Dr. Stevenson requested an historical perspective on the development of the human diploid cell strains, in particular WI-38 with no technical details, since they can be found in the literature (14, 19). He requested “introspection that may yield some interesting insights into the process of scientific thought and motivation of scientists … because the scientific literature seldom contains such information and future generations of scientists may never know this important and often misunderstood background of thinking and motivation unless you tell it directly. Also, in retrospect, how do you feel now about your approach? And what would you do differently today, given your interim experience and the current state of the art? In sum, this is a license to philosophize and distill your wisdom.”The invitation to present this paper could not have come at a more propitious time. Believe it or not, this year marks the twenty-first birthday of WI-38. The cells have reached their majority. Since they are normal human cells, they actually fulfill all the criteria necessary to obtain a voting registration card. Indeed, they are the first cultured normal human cell population to ever reach voting age. But, alas, they contain no brain cells. However, that never was a requirement for voting rights in this country.
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Authors: Shay, J. W., & Wright, W. E.
Affiliations: The University of Texas Southwestern Medical Center (US)
Corresponding author: Shay, Jerry W.
ORCID: Shay, Jerry W.
Wright, Woodring E.
Venue: Nature Reviews Molecular Cell Biology
Publisher: Springer Science and Business Media LLC
Published: 2000-10
Volume: 1
Issue: 1
Pages: 72-76
ISSN: 1471-0072 (ISSN-L)
1471-0080
DOI: 10.1038/35036093
OpenAlex: W1517051009
Cited by: 764
References: 48
Citations by year: 2026: 24 · 2025: 44 · 2024: 72 · 2023: 64 · 2022: 51 · 2021: 44 · 2020: 49 · 2019: 37 · 2018: 31 · 2017: 40 · 2016: 37 · 2015: 29 · 2014: 26 · 2013: 19 · 2012: 17
FWCI: 1.47
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Nature Reviews Molecular Cell Biology (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Microtubule and mitosis dynamics
Keywords: Hayflick limit, cellular senescence, cellular aging, replicative lifespan, human cell culture
MeSH terms: Aging, Cell Division, Cells, Cultured, Humans, Time Factors, United States, Telomere, Cellular Senescence, Telomerase, History, 19th Century, History, 20th Century, History, 21st Century

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Hayflick, his limit, and cellular ageing

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