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About Biomedical Basics
Biomedical Basics are AI-generated explanations prepared with access to the complete collection, human-reviewed prior to publication. Short and simple, covering biomedical and life sciences fundamentals.
Topics Covered
- Cellular aging mechanisms
- Telomere shortening & DNA damage
- Senescence-associated secretory phenotype
- Senescence in tumor suppression & disease
- Senescent cells in inflammation & aging
- Senescence impacts tissue regeneration
- Senolytics for healthy aging
Talk Citation
(2025, November 30). Cell senescence and ageing [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 4, 2025, from https://doi.org/10.69645/JZCV6821.Export Citation (RIS)
Publication History
- Published on November 30, 2025
Financial Disclosures
Transcript
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0:00
The topic of Cell Senescence and
Aging will be explored
through the basic mechanisms
of cellular aging, focusing on
how telomere shortening and
DNA damage drive cells
into senescence.
We will discuss how senescent
cells, through changes like
the senescence-associated
secretory
phenotype (SASP), disrupt
tissue function
and contribute to
chronic inflammation
and age-related diseases.
The dual role of senescence—as
both a tumor-suppressing process and
a contributor to disease—will be examined.
Finally, we will consider
emerging approaches, such as
senolytic therapies,
aimed at targeting
senescent cells to
promote healthy aging..
Aging is a universal process
marked by a gradual loss of
physiological integrity and
rising vulnerability
to disease and death.
Rather than a single cause,
aging results from accumulated
cellular and molecular damage.
Senescence, where cells
cease dividing and show
distinct biochemical changes, is
central to aging and disease.
This lecture will explore
the mechanisms of
cellular aging,
the role of
telomeres, DNA damage,
and how these contribute to
tissue dysfunction and disease.
To understand cell senescence,
we examine the key drivers
of cellular aging.
Telomere shortening is a
major factor—progressive loss
of protective DNA-protein
structures at chromosome ends.
Each DNA replication round
causes telomere
erosion, leading to
critically short
telomeres seen as
DNA damage,
triggering permanent cell cycle arrest.