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Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

1 Jan 2017Review

Linking telomere loss and mitochondrial dysfunction in chronic disease

Ana Carlota Gonzalez-Ebsen 1,*, Niels Gregersen 1, Rikke K.J. Olsen 1
Affiliation
Article Info

1 Research Unit for Molecular Medicine, Department for Clinical Medicine, Aarhus University and Aarhus University Hospital, Palle Juul-Jensens Boulevard 99, 8200 Aarhus N, Denmark

Abstract

Telomeres and mitochondria are known to deteriorate over time. Telomere shortening is associated with aging, early senescence, and premature cell death. Mitochondrial dysfunction produces indiscriminate amounts of reactive oxygen species that may lead to oxidative damage to cellular constituents, including telomeric DNA, causing telomere shortening. In fact, patients with primary mitochondrial dysfunction (for example respiratory chain disorders) and secondary mitochondrial dysfunction (such as metabolic diseases, neurodegenerative diseases, cardiovascular diseases, and mood disorders, among others) have shorter telomeres compared to those of healthy controls. Drawing a mechanistic connection between telomere function and mitochondria biology will provide a broader perspective for understanding the pathophysiology of diseases and their relation to the aging process, and may provide opportunities for new possible treatments.

Keywords

  • Telomeres
  • Mitochondrial Dysfunction
  • Oxidative Stress
  • Chronic Diseases
  • Review

References