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Stress and the epigenetic landscape: a link to the pathobiology of human diseases?

Nature Reviews Genetics volume 11, pages 806–812 (2010)Cite this article

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Abstract

Accumulating evidence points to a major role for chronic stress of cell renewal systems in the pathogenesis of important human diseases, including cancer, atherosclerosis and diabetes. Here we discuss emerging evidence that epigenetic abnormalities may make substantial contributions to these stress-induced pathologies. Although the mechanisms remain to be fully elucidated, we suggest that chronic stress can elicit heritable changes in the chromatin landscape that 'lock' cells in abnormal states, which then lead to disease. We emphasize the need to investigate epigenetic states in disease and links to stress and to consider how the knowledge gained through these studies may foster new means of disease prevention and management.

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Figure 1: The effect of stress on cell renewal systems.
Figure 2: Perturbations caused by chronic stress.

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Acknowledgements

The authors thank members of the Baylin laboratory for helpful suggestions and reading of the manuscript and K. Bender for help with manuscript preparation. Portions of the authors' work cited have been supported by the National Cancer Institute grant CA043318, the National Institute of Environmental Health Sciences grant ES011858 and the National Institutes of Health grant CA116160.

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  1. Sarah E. Johnstone and Stephen B. Baylin are at The Sidney Kimmel Cancer Research Center at Johns Hopkins, Bunting Blaustein Cancer Research Building, 1650 Orleans Street, Suite 544, Baltimore, Maryland 21231-1000, USA.,

    Sarah E. Johnstone & Stephen B. Baylin

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Correspondence to Stephen B. Baylin.

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Glossary

Amyloid plaque

A focal extracellular collection of amyloid protein that surrounds dystrophic neurites in the hippocampus, amygdala and neocortex.

Committed progenitor cell

A multipotent cell that is committed to a particular lineage and incapable of self-renewal.

Histone post-translational modification

A covalent alteration of a histone tail residue that alters chromatin structure. Modifications include phosphorylation, methylation, acetylation, sumoylation and ubiquitylation.

Histone variant

A histone that differs from canonical histones in terms of its structure and regulation.

Neoplasia

The abnormal proliferation of cells. A neoplasm can be further characterized as benign or malignant based on its ability to invade other tissues.

Neurofibrillary tangle

A filamentous bundle of tau protein that aggregates in the cytoplasm of neurons and is a histological hallmark of Alzheimer's disease.

Nucleosome remodelling

An enzymatic process that alters the position of nucleosomes and can influence chromatin condensation.

Peripheral resistance

The resistance of the peripheral vasculature to blood flow.

Polycomb group

A family of proteins that are involved in gene silencing during development through methylation of histone H3 lysine 27.

Pre-malignant

A state in which a cell is benign but poised to become malignant.

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Johnstone, S., Baylin, S. Stress and the epigenetic landscape: a link to the pathobiology of human diseases?. Nat Rev Genet 11, 806–812 (2010). https://doi.org/10.1038/nrg2881

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