Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

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...
Mitochondria01:37

Mitochondria

Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
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...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a rapamycin-insensitive companion...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Remembrance of things past: Towards a life-course biology of aging.

PLoS biology·2026
Same author

Evolutionary genetics of ageing.

Nature reviews. Genetics·2026
Same author

ß-adrenergic-like signalling engages CrebB in Drosophila gut to promote female longevity.

Nature communications·2026
Same author

Dietary restriction in aging and longevity.

Nature aging·2026
Same author

Past, present and future perspectives on the science of aging.

Nature aging·2026
Same author

Loss of Pol III repressor Maf1 in neurons promotes longevity by preventing the age-related decline in 5S rRNA and translation.

PLoS biology·2025

Related Experiment Video

Updated: May 30, 2026

Techniques to Induce and Quantify Cellular Senescence
06:51

Techniques to Induce and Quantify Cellular Senescence

Published on: May 1, 2017

Death and dessert: nutrient signalling pathways and ageing.

Nazif Alic1, Linda Partridge

  • 1Institute of Healthy Ageing, and GEE, University College London, London WC1E 6BT, UK.

Current Opinion in Cell Biology
|August 13, 2011
PubMed
Summary

Reducing nutrient intake without malnutrition can delay aging and extend healthspan across species. Targeting nutrient signaling pathways offers a promising strategy for interventions into human aging and related diseases.

More Related Videos

SA-β-Galactosidase-Based Screening Assay for the Identification of Senotherapeutic Drugs
07:39

SA-β-Galactosidase-Based Screening Assay for the Identification of Senotherapeutic Drugs

Published on: June 28, 2019

Related Experiment Videos

Last Updated: May 30, 2026

Techniques to Induce and Quantify Cellular Senescence
06:51

Techniques to Induce and Quantify Cellular Senescence

Published on: May 1, 2017

SA-β-Galactosidase-Based Screening Assay for the Identification of Senotherapeutic Drugs
07:39

SA-β-Galactosidase-Based Screening Assay for the Identification of Senotherapeutic Drugs

Published on: June 28, 2019

Area of Science:

  • Gerontology
  • Molecular Biology
  • Nutritional Science

Background:

  • Nutrient intake reduction without malnutrition is a conserved mechanism to delay aging and extend healthspan.
  • This phenomenon is observed across diverse organisms, from yeast to primates.
  • Nutrient signaling pathways play a crucial role in mediating these aging effects.

Purpose of the Study:

  • To review current knowledge on the interactions between nutrient signaling pathways and aging.
  • To focus on recent findings (past few years) in this field.
  • To highlight the potential of these pathways as targets for human aging interventions.

Main Methods:

  • Literature review of recent scientific findings.
  • Analysis of studies investigating nutrient intake, aging, and related diseases.
  • Focus on genetic and pharmacological interventions targeting nutrient signaling pathways.

Main Results:

  • Nutrient signaling pathways are key mediators of aging.
  • Genetic or pharmacological dampening of these pathways can recapitulate the life-extending effects of reduced nutrient intake.
  • These pathways represent promising targets for therapeutic interventions.

Conclusions:

  • Interventions targeting nutrient signaling pathways hold significant potential for delaying human aging.
  • Further research into these pathways could lead to novel strategies for combating age-related diseases.
  • Understanding these molecular mechanisms is crucial for developing effective anti-aging therapies.