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Related Concept Videos

Replicative Cell Senescence02:15

Replicative Cell Senescence

Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds the telomeric...
Replicative Cell Senescence02:15

Replicative Cell Senescence

Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds the telomeric...
Telomeres and Telomerase02:41

Telomeres and Telomerase

In eukaryotic DNA replication, a single-stranded DNA fragment remains at the end of a chromosome after the removal of the final primer. This section of DNA cannot be replicated in the same manner as the rest of the strand because there is no 3’ end to which the newly synthesized DNA can attach. This non-replicated fragment results in gradual loss of the chromosomal DNA during each cell duplication. Additionally, it can induce a DNA damage response by enzymes that recognize single-stranded DNA.
Aging01:26

Aging

Aging is a complex biological phenomenon influenced by various processes that affect cellular and systemic functions. Several prominent theories attempt to explain its mechanisms, highlighting cellular limitations, oxidative damage, and hormonal changes as central factors in aging.
Cellular Clock Theory
The cellular clock theory posits that the human lifespan is closely tied to the finite capacity of cells to divide, a phenomenon governed by telomeres, which are protective caps at the ends of...
Methods of Nuclear Reprogramming01:24

Methods of Nuclear Reprogramming

Nuclear reprogramming is a process of transforming one cell type into an unrelated cell type by epigenetic changes that alter the cell’s original gene expression pattern. Such epigenetic changes force cells to express a different set of genes, which play a significant role in inducing transformation into other cell types. Nuclear reprogramming offers applications in reproductive cloning for livestock propagation and regenerative medicine — developing patient-specific cells for injury repair.
Replication in Eukaryotes01:29

Replication in Eukaryotes

In eukaryotic cells, DNA replication is highly conserved and tightly regulated. Multiple linear chromosomes must be duplicated with high fidelity before cell division, so there are many proteins that fulfill specialized roles in the replication process. Replication occurs in three phases: initiation, elongation, and termination, and ends with two complete sets of chromosomes in the nucleus.
Many Proteins Orchestrate Replication at the Origin
Eukaryotic replication follows many of the same...

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A Suppressor Screen for the Characterization of Genetic Links Regulating Chronological Lifespan in Saccharomyces cerevisiae
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Turning back time: a comprehensive list of interventions that decrease next-generation epigenetic aging clocks in

Adiv A Johnson1, David A Sinclair2

  • 1Tally Health, New York, NY, United States.

Frontiers in Genetics
|June 15, 2026
PubMed
Summary
This summary is machine-generated.

Next-generation epigenetic clocks track biological age. Many interventions, including exercise and diet, can reduce epigenetic age, offering new avenues for longevity research and healthspan.

Keywords:
aging biomarkerbiohorologyclinical trialsepigenetic age reversalepigenetic aging clocknext-generation clock

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Area of Science:

  • Biogerontology
  • Epigenetics
  • Molecular Biology

Background:

  • Epigenetic aging clocks estimate biological age using DNA methylation patterns.
  • Next-generation clocks offer improved accuracy and stronger links to mortality risk compared to earlier models.
  • Understanding interventions that modify epigenetic age is crucial for longevity and healthspan research.

Purpose of the Study:

  • To systematically review human studies on interventions affecting next-generation epigenetic clocks.
  • To identify interventions that can decrease or accelerate epigenetic age.
  • To analyze effect sizes and compare clock responsiveness to various interventions.

Main Methods:

  • Conducted systematic literature searches across multiple databases.
  • Included 41 human studies reporting effects of interventions on next-generation epigenetic clocks.
  • Analyzed data on pharmaceutical, lifestyle, supplementation, and other interventions.

Main Results:

  • Diverse interventions, including exercise, plant-rich diets, semaglutide, caloric restriction, and pitavastatin, decreased epigenetic age.
  • Nicotinamide riboside, rapamycin, and senolytics showed no significant effect.
  • Plasmapheresis and certain other therapeutics were found to accelerate epigenetic aging.

Conclusions:

  • Next-generation epigenetic clocks can be modified by a wide array of interventions.
  • Lifestyle and pharmaceutical interventions show promise in reducing epigenetic age.
  • Further research is warranted to optimize interventions for healthy aging and longevity.