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Related Experiment Video

Updated: Jun 2, 2026

Quantifying Tissue-Specific Proteostatic Decline in Caenorhabditis elegans

Quantifying Tissue-Specific Proteostatic Decline in Caenorhabditis elegans

Published on: September 7, 2021

Transposable elements in aging: From biomarkers to effectors.

Alejandro Fuentes-Iglesias¹, Raquel García-Vílchez¹, Diana Guallar¹

¹Epitranscriptomics & Ageing laboratory, Center for Research in Molecular Medicine and Chronic Diseases (CiMUS), Universidade de Santiago de Compostela (USC), Santiago de Compostela, Spain.

Advances in Genetics

|June 1, 2026

Summary

This summary is machine-generated.

Transposable elements (TEs), once dismissed as "junk DNA," are now understood to drive aging by causing genomic instability and inflammation. Therapeutic strategies targeting TE dysregulation show promise for extending lifespan and promoting healthy aging.

Keywords:

Aging DNA methylation Epigenetic regulation Heterochromatin Inflammaging Innate immunity LINE-1 Retrotransposon Transposable element

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Last Updated: Jun 2, 2026

Quantifying Tissue-Specific Proteostatic Decline in Caenorhabditis elegans

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Measurement of Protein Turnover Rates in Senescent and Non-Dividing Cultured Cells with Metabolic Labeling and Mass Spectrometry

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Published on: April 6, 2022

Area of Science:

Genomics
Aging Research
Molecular Biology

Background:

Transposable elements (TEs) comprise a significant portion of mammalian genomes.
Far from being

Purpose of the Study:

To review the role of transposable elements (TEs) in aging.
To discuss epigenetic regulation of TEs and their activation during aging.
To explore therapeutic strategies and biomarkers related to TE dysregulation in aging.

Main Methods:

Review of current scientific literature on transposable elements and aging.
Analysis of epigenetic mechanisms controlling TE silencing.
Examination of evidence for TE activation during physiological aging.
Discussion of therapeutic interventions and biomarker potential.

Main Results:

Aging is linked to heterochromatin loss, leading to TE derepression.
TE activation causes genomic instability and perpetuates inflammatory responses via DNA and RNA sensors (e.g., cGAS-STING, RIG-I, MDA5).
Therapeutic interventions like NRTI, lifestyle changes, and SIRT6 activation can mitigate TE dysregulation effects.

Conclusions:

TE dysregulation is a fundamental mechanism of aging.
Targeting TEs offers a promising therapeutic avenue for healthy aging.
TE-based biomarkers are valuable for assessing biological age and disease risk.