Epigenetic Programming of Synthesis, Release, and/or Receptor Expression of Common Mediators Participating in the Risk/Resilience for Comorbid Stress-Related Disorders and Coronary Artery Disease

Campo, Carlos Manuel Zapata-Martín del; Martínez-Rosas, Martín; Guarner-Lans, Verónica

doi:10.3390/ijms19041224

Cited by 43 publications

(22 citation statements)

References 206 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Corticotrophin releasing factor, vasopressin, oxytocin, natriuretic hormones, angiotensin, neuregulins, some purinergic substances and some cytokines contribute to long-term modulation and restructuring of cardiovascular regulation networks. The synthesis, release and receptor expression of these mediators seem to be under epigenetic control since early stages of life [70,156].…”

Section: Exposure To Chronic Stressmentioning

confidence: 99%

Early Programming of Adult Systemic Essential Hypertension

Guarner-Lans

Ramírez-Higuera²,

Rubio-Ruiz

et al. 2020

IJMS

Self Cite

View full text Add to dashboard Cite

Cardiovascular diseases are being included in the study of developmental origins of health and disease (DOHaD) and essential systemic hypertension has also been added to this field. Epigenetic modifications are one of the main mechanisms leading to early programming of disease. Different environmental factors occurring during critical windows in the early stages of life may leave epigenetic cues, which may be involved in the programming of hypertension when individuals reach adulthood. Such environmental factors include pre-term birth, low weight at birth, altered programming of different organs such as the blood vessels and the kidney, and living in disadvantageous conditions in the programming of hypertension. Mechanisms behind these factors that impact on the programming include undernutrition, oxidative stress, inflammation, emotional stress, and changes in the microbiota. These factors and their underlying causes acting at the vascular level will be discussed in this paper. We also explore the establishment of epigenetic cues that may lead to hypertension at the vascular level such as DNA methylation, histone modifications (methylation and acetylation), and the role of microRNAs in the endothelial cells and blood vessel smooth muscle which participate in hypertension. Since epigenetic changes are reversible, the knowledge of this type of markers could be useful in the field of prevention, diagnosis or epigenetic drugs as a therapeutic approach to hypertension.

show abstract

Section: Exposure To Chronic Stressmentioning

confidence: 99%

Early Programming of Adult Systemic Essential Hypertension

Guarner-Lans

Ramírez-Higuera²,

Rubio-Ruiz

et al. 2020

IJMS

Self Cite

View full text Add to dashboard Cite

show abstract

“…Modifications of the genomic expression of proteins controlling mitochondrial function, protein folding in the ER and nuclear processes such as telomere length determination and DNA repair might be, in part, the basis of the common susceptibility (or resilience) to develop CMD and NPD. Particularly, adverse early life experiences significantly contribute to the possibility of developing CMD and NPD later in life in when adulthood is reached [ 9 ]. Neurodegenerative diseases have many known environmental risk factors, and there is evidence that early life exposure can increase the risk of the condition later in life.…”

Section: Introductionmentioning

confidence: 99%

Epigenetics of Subcellular Structure Functioning in the Origin of Risk or Resilience to Comorbidity of Neuropsychiatric and Cardiometabolic Disorders

Campo¹,

Martínez-Rosas²,

Guarner-Lans³

2018

IJMS

Self Cite

View full text Add to dashboard Cite

Mechanisms controlling mitochondrial function, protein folding in the endoplasmic reticulum (ER) and nuclear processes such as telomere length and DNA repair may be subject to epigenetic cues that relate the genomic expression and environmental exposures in early stages of life. They may also be involved in the comorbid appearance of cardiometabolic (CMD) and neuropsychiatric disorders (NPD) during adulthood. Mitochondrial function and protein folding in the endoplasmic reticulum are associated with oxidative stress and elevated intracellular calcium levels and may also underlie the vulnerability for comorbid CMD and NPD. Mitochondria provide key metabolites such as nicotinamide adenine dinucleotide (NAD+), ATP, α-ketoglutarate and acetyl coenzyme A that are required for many transcriptional and epigenetic processes. They are also a source of free radicals. On the other hand, epigenetic markers in nuclear DNA determine mitochondrial biogenesis. The ER is the subcellular organelle in which secretory proteins are folded. Many environmental factors stop the ability of cells to properly fold proteins and modify post-translationally secretory and transmembrane proteins leading to endoplasmic reticulum stress and oxidative stress. ER functioning may be epigenetically determined. Chronic ER stress is emerging as a key contributor to a growing list of human diseases, including CMD and NPD. Telomere loss causes chromosomal fusion, activation of the control of DNA damage-responses, unstable genome and altered stem cell function, which may underlie the comorbidity of CMD and NPD. The length of telomeres is related to oxidative stress and may be epigenetically programmed. Pathways involved in DNA repair may be epigenetically programmed and may contribute to diseases. In this paper, we describe subcellular mechanisms that are determined by epigenetic markers and their possible relation to the development of increased susceptibility to develop CMD and NPD.

show abstract

“…alternative pathways and mechanisms, including epigenetic control of gene expression, have been raised to explain the relationship between chronic stress and CVD (8,9).…”

mentioning

confidence: 99%

Contribution of DNA methylation in chronic stress‐induced cardiac remodeling and arrhythmias in mice

Zhang¹,

Li²,

Liu³

et al. 2019

The FASEB Journal

View full text Add to dashboard Cite

It is recognized that stress can induce cardiac dysfunction, but the underlying mechanisms are not well understood. The present study aimed to test the hypothesis that chronic negative stress leads to alterations in DNA methylation of certain cardiac genes, which in turn contribute to pathologic remodeling of the heart. We found that mice that were exposed to chronic restraint stress (CRS) for 4 wk exhibited cardiac remodeling toward heart failure, as characterized by ventricular chamber dilatation, wall thinning, and decreased contractility. CRS also induced cardiac arrhythmias, including intermittent sinus tachycardia and bradycardia, frequent premature ventricular contraction, and sporadic atrioventricular conduction block. Circulating levels of stress hormones were elevated, and the cardiac expression of tyrosine hydroxylase, a marker of sympathetic innervation, was increased in CRS mice. Using reduced representation bisulfite sequencing, we found that although CRS did not lead to global changes in DNA methylation in the murine heart, it nevertheless altered methylation at specific genes that are associated with the dilated cardiomyopathy (DCM) (e.g., desmin) and adrenergic signaling of cardiomyocytes (ASPC) (e.g., adrenergic receptor‐α1) pathways. We conclude that CRS induces cardiac remodeling and arrhythmias, potentially through altered methylation of myocardial genes associated with the DCM and ASPC pathways.—Zhang P., Li, T., Liu, Y.‐Q., Zhang, H., Xue, S.‐M., Li, G., Cheng, H.‐Y.M., Cao, J.‐M. Contribution of DNA methylation in chronic stress‐induced cardiac remodeling and arrhythmias in mice. FASEB J. 33, 12240‐12252 (2019). http://www.fasebj.org

show abstract

Epigenetic Programming of Synthesis, Release, and/or Receptor Expression of Common Mediators Participating in the Risk/Resilience for Comorbid Stress-Related Disorders and Coronary Artery Disease

Cited by 43 publications

References 206 publications

Early Programming of Adult Systemic Essential Hypertension

Early Programming of Adult Systemic Essential Hypertension

Epigenetics of Subcellular Structure Functioning in the Origin of Risk or Resilience to Comorbidity of Neuropsychiatric and Cardiometabolic Disorders

Contribution of DNA methylation in chronic stress‐induced cardiac remodeling and arrhythmias in mice

Contact Info

Product

Resources

About