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Global Translational Medicine Epigenetics on cardiovascular diseases

This dark genome serves as a fundamental regulator in diverse biological substances and proteins capable of
the decoding process, or expression, of protein-making binding to DNA, regulating functions such as activating
genes. Moreover, it exerts control over “how our genes or suppressing genes and directing the synthesis of
behave in response to all the environmental pressures our novel proteins. Environmental and behavioral stimuli
bodies face throughout our lives, ranging from diet to can leverage epigenetic regulatory processes in gene
stress, pollution, exercise, and how much we sleep, a field expression, impacting certain disorders, and increasing
known as epigenetics .” Atherosclerosis is characterized their risk by altering primary genetic predisposition . In
[6]
[1]
as a chronic inflammatory disease involving large to CVDs, numerous epigenetic modifications are implicated,
medium-sized coronary or peripheral arteries, marked yet despite advancements in epigenetic research over the
by progressive and complex arterial changes. Clinically, past 50 years, clinical applications remain unsatisfactory .
[7]
associated atherosclerotic plaques emerge, leading to The connection between external risk factors, such
cardiovascular diseases (CVDs). In this review, the terms as environmental elements and behavioral manners,
coronary artery disease (CAD) and chronic progressive and sequence-independent heritable DNA changes is
CVD are used interchangeably. Epigenetic research has significant. This connection induces significant changes in
expanded into the cardiovascular domain, aiming to reveal cellular differentiation and function, influencing the health
[8]
complex network interconnections between epigenetic and adaptability of the organism .
processes and the genesis and progression of CVDs. The The role of genetics is evident in certain
subjects of acute myocardial infarction (AMI) and heart cardiomyopathies, particularly in cases related to mutations
failure (HF) are sporadically referenced in this context. in specific genes linked to the sarcomere. However, in
Clinically, relevant arterial plaques entail the interaction complex CVDs, genetic changes are more intricate and
of different cells that give rise to infiltration of immune challenging to comprehend, often perpetuating from one
cells, dysfunction in endothelial cells, proliferation of generation of cells to the next . Epigenetic mechanisms
[9]
vascular smooth muscle cells (VSMCs), activation of and factors collectively establish a mechanistic link between
monocytes and macrophages, and the formation of foam environmental exposures transmitted through epigenetic
cells. Additional significant factors contributing to the mechanisms and gene expression profiles, influencing the
development of cardiovascular events include oxidative development and progression of CVDs. Consequently,
stress and certain coronary hemodynamic parameters the epigenome presents novel categories of therapeutic
(coronary vessel wall thickening and wall shear stress). targets [9,10] . Perrino et al. , in a “Position Paper,” propose
[11]
Non-coding RNAs (ncRNAs), encompassing short the integration of epigenomic and transcriptomic data
non-coding RNAs (microRNAs or miRNAs), long non- as an advantageous procedure to identify crucial disease
coding RNAs (lncRNAs), and circular non-coding RNAs networks in patients with CVDs. They underline the
(circRNAs) have been identified as crucial mechanistic potentials and limitations of these procedures and endorse
regulators of messenger RNA (mRNA) and protein innovative diagnostic or therapeutic targets, particularly
expression, potentially contributing to atherosclerosis . for acute ischemia or reperfusion injury and ischemic
[2]
The term “epigenetics” is interpreted as the inquiry of HF in the post-genomic stage. At present, routine clinical
inheritable and transient changes in gene expressions and practice predominantly employs a reductionist approach
phenotypes without altering the normal DNA sequence. to diagnosis and treatment [7,12] . The holistic methodology
It encompasses genomic mechanisms regulating gene of SB, incorporated into everyday clinical practice, is
expression and is associated with chemical modifications envisioned as a more relevant and personalized diagnostic
of DNA or responses to environmental and behavioral and therapeutic approach, considering presumed genes
changes. The involved genomic mechanisms comprise and molecular networks underlying CVDs .
[13]
DNA methylation, histone modifications, and RNA- In this review, we underscore several key facets: (i) the
based mechanisms . According to Alghamdi et al. , epigenetic regulatory mechanisms linked to cardiovascular
[3]
[4]
epigenetics is the exploration of inheritable changes in risk factors and their effect on our understanding of
gene expressions and phenotypes primarily resulting from CVDs, (ii) the potential for epigenetic changes to affect
alterations in chromatin or its packaging, thereby changing the clinical cardiovascular phenotype, thereby expanding
DNA accessibility. our opportunities for novel diagnostic and therapeutic
Comprehending regulatory elements, such as approaches, (iii) the broader implications of epigenetics
enhancers and promoters, is crucial in deciphering cell in diverse research domains such as the environment and
type-specific gene expression patterns that instigate social sciences, (iv) the involvement of epigenetics in the
diseases in complex tissues . The epigenome comprises ongoing conflict between the gene-based reductionist
[5]

Volume 2 Issue 4 (2023) 2 https://doi.org/10.36922/gtm.1868