DNA repair fidelity in stem cell maintenance, health, and disease

Chinnadurai Mani, P (Hemachandra) Reddy, Komaraiah Palle

Research output: Contribution to journalReview article

Abstract

Stem cells are a sub population of cell types that form the foundation of our body, and have the potential to replicate, replenish and repair limitlessly to maintain the tissue and organ homeostasis. Increased lifetime and frequent replication set them vulnerable for both exogenous and endogenous agents-induced DNA damage compared to normal cells. To counter these damages and preserve genetic information, stem cells have evolved with various DNA damage response and repair mechanisms. Furthermore, upon experiencing irreparable DNA damage, stem cells mostly prefer early senescence or apoptosis to avoid the accumulation of damages. However, the failure of these mechanisms leads to various diseases, including cancer. Especially, given the importance of stem cells in early development, DNA repair deficiency in stem cells leads to various disabilities like developmental delay, premature aging, sensitivity to DNA damaging agents, degenerative diseases, etc. In this review, we have summarized the recent update about how DNA repair mechanisms are regulated in stem cells and their association with disease progression and pathogenesis.

Original languageEnglish (US)
JournalBiochimica et Biophysica Acta - Molecular Basis of Disease
DOIs
StatePublished - Jan 1 2019
Externally publishedYes

Fingerprint

DNA Repair
Stem Cells
Maintenance
Health
DNA Damage
DNA Repair-Deficiency Disorders
Premature Aging
Developmental Disabilities
Disease Progression
Homeostasis
Apoptosis
DNA
Population
Neoplasms

Keywords

  • Disease
  • DNA damage and repair
  • Gene Therapy
  • Stem cells

ASJC Scopus subject areas

  • Molecular Medicine
  • Molecular Biology

Cite this

DNA repair fidelity in stem cell maintenance, health, and disease. / Mani, Chinnadurai; Reddy, P (Hemachandra); Palle, Komaraiah.

In: Biochimica et Biophysica Acta - Molecular Basis of Disease, 01.01.2019.

Research output: Contribution to journalReview article

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