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RESEARCH PAPER / 2026-08-06

The role of transposable elements-endogenous retroviruses in embryonic development and regeneration.

Ziyan Li, Yixin Huang, Zhenyu Ju, Rongrong Le, Zhiyang Chen

Key Laboratory of Regenerative Medicine of Ministry of Education, Institute of Aging and Regenerative Medicine, Department of Developmental & Regenerative Medicine, College of Life Science and Technology, Jinan University, No. 601, Huangpu Avenue West, Tianhe District, Guangzhou 510632, China.Key Laboratory of Regenerative Medicine of Ministry of Education, Institute of Aging and Regenerative Medicine, Department of Developmental & Regenerative Medicine, College of Life Science and Technology, Jinan University, No. 601, Huangpu Avenue West, Tianhe District, Guangzhou 510632, China. · pubmed

Abstract

Endogenous retroviruses (ERVs) are dynamically regulated across the lifespan and can function as context-dependent components of host gene-regulatory networks. During embryonic development, selected ERV-derived elements are co-opted to support zygotic genome activation, lineage specification, and placental development. In adult tissues, ERV-derived sequences can contribute to tissue and immune homeostasis, whereas potentially disruptive ERV activity is constrained by epigenetic mechanisms. During regeneration and somatic cell reprogramming, ERV and broader transposable-element programs undergo transient, locus-specific remodeling. In aging, the weakening of epigenetic and nuclear restraint can promote aberrant ERV derepression, inflammation, and functional decline. This review summarizes the diverse roles of ERVs across these contexts and discusses the challenges of defining locus-specific functions, resolving repetitive sequences, and developing safe ERV-targeted interventions.

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

This review synthesizes existing evidence that endogenous retroviruses contribute to aging phenotypes through epigenetic instability and inflammation, suggesting that targeting ERV derepression could mitigate age-related functional decline. The paper is relevant because it addresses a potential root cause of aging (epigenetic drift and genomic instability) rather than just treating symptoms, but as a review summarizing known mechanisms without presenting new experimental data or a novel therapeutic breakthrough, its immediate scientific impact is limited to incremental synthesis of the field.

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