DNA methylation and atherosclerosis prevention

Decoding Atherosclerosis: How DNA Methylation Holds the Key to Prevention

Lena Voss in Health & Wellness August 2025 • 4 min read.

"Unlocking the secrets of DNA methylation could revolutionize our approach to preventing and treating heart disease. Discover the latest insights into this cutting-edge field."

For over a century, scientists have been unraveling the complexities of cardiovascular diseases (CVD), and new discoveries at the molecular level continue to reshape our understanding. While genetics play a role, explaining only a fraction of the risk, the dynamics of epigenome modifications, particularly DNA methylation, are emerging as key players in reshaping pathological processes in CVD.

DNA methylation, a major epigenetic regulator, influences cell-type specific gene expression in mural cells. However, the precise role of DNA methylation, specifically hyper- and hypomethylation, in CVD pathology remains a topic of intense investigation. Recent research suggests that DNA hypomethylation, the loss of methyl cytosines, is a prominent feature of atherosclerosis, while certain genes become hypermethylated as the disease advances in medium-sized and large arteries.

This article highlights recent, groundbreaking findings that connect alterations in DNA methylation to atherogenesis, the development of fatty plaques in arteries. By exploring these connections, we can identify potential new avenues for treatments and preventative measures, opening doors to a future where personalized interventions mitigate the risk of heart disease.

DNA Methylation: The Conductor of Gene Expression in Atherosclerosis

DNA methylation and atherosclerosis prevention

DNA methylation is a dynamic process that involves adding or removing methyl groups to DNA, thereby affecting gene expression without altering the underlying DNA sequence. This process is crucial in regulating various cellular functions, and its dysregulation has been implicated in numerous diseases, including atherosclerosis.

Here's a closer look at the key aspects of DNA methylation in the context of atherosclerosis:

De Novo Methylation: Carried out by DNMT3A/3B, this process establishes new methylation patterns, particularly during embryonic development. However, ongoing de novo methylation also occurs in adults, contributing to the evolving landscape of DNA methylation in atherosclerosis.
Maintenance of Methylation: DNMT1 ensures that methylation patterns are faithfully copied during cell division, preserving cell identity and function. However, this process can also perpetuate aberrant methylation patterns in diseased cells.
Demethylation: TET1-3 enzymes oxidize 5mC to 5hmC, 5fC, and 5caC, which can then be removed via the base-excision repair (BER) pathway. Demethylation plays a critical role in activating enhancers and promoting chromatin unfolding, influencing gene expression in atherosclerosis.
Readers, Writers, and Erasers: The interplay of methyl cytosine writers, readers, and erasers determines the overall DNA methylation landscape. Disruptions in this balance can lead to altered gene expression and contribute to the development of atherosclerotic lesions.

Understanding the intricate mechanisms of DNA methylation provides valuable insights into the pathogenesis of atherosclerosis. By targeting these processes, we may be able to develop novel therapeutic strategies to prevent and treat this widespread disease.

The Future of Atherosclerosis Treatment: Targeting DNA Methylation

As research continues to unravel the complexities of DNA methylation in atherosclerosis, promising new therapeutic avenues are emerging. Interventions that target DNA methylation processes, such as stimulating mitochondrial biogenesis, preventing cellular senescence, and restoring the epigenetic clock, hold great potential for preventing and treating this disease. While challenges remain, the future of atherosclerosis treatment lies in harnessing the power of epigenetics to develop personalized and effective therapies.

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Everything You Need To Know

What is Atherosclerosis, and how does it relate to the research on DNA methylation?

Atherosclerosis is a leading cause of cardiovascular disease, and it is much more than just clogged arteries. This condition involves the buildup of fatty plaques in the arteries. Research has found that DNA methylation plays a significant role in the development of atherosclerosis. Specifically, changes in DNA methylation patterns, such as hypermethylation and hypomethylation, are linked to the progression of the disease. Understanding these connections is crucial for developing new treatments and preventative measures.

How does DNA methylation influence gene expression, and why is it important in the context of Atherosclerosis?

DNA methylation is a dynamic process that involves adding or removing methyl groups to DNA, influencing gene expression without changing the DNA sequence. In the context of atherosclerosis, DNA methylation patterns, including hypermethylation and hypomethylation, play a critical role in regulating the expression of genes involved in the disease process. Aberrant methylation patterns can lead to altered gene expression, contributing to the development of atherosclerotic lesions and the progression of the condition. Dysregulation of DNA methylation can impact cell-type specific gene expression in mural cells, further affecting the pathology.

What are the key processes of DNA methylation, and how do they contribute to the development of Atherosclerosis?

The key processes involved in DNA methylation include de novo methylation by DNMT3A/3B, maintenance of methylation by DNMT1, and demethylation by TET1-3 enzymes. De novo methylation establishes new methylation patterns, while DNMT1 ensures existing patterns are copied during cell division. Demethylation removes methyl groups. These processes involve methyl cytosine writers, readers, and erasers. In atherosclerosis, imbalances in these processes, such as hypomethylation, can lead to altered gene expression, contributing to the formation of fatty plaques in the arteries. For instance, hypomethylation, the loss of methyl cytosines, is a prominent feature of atherosclerosis, while certain genes become hypermethylated as the disease advances.

Can you explain the role of 'Readers, Writers, and Erasers' in the context of DNA methylation and Atherosclerosis?

In DNA methylation, 'Writers' are enzymes like DNMT3A/3B that add methyl groups to DNA, establishing new methylation patterns. 'Readers' are proteins that recognize and bind to methylated DNA, influencing gene expression. 'Erasers,' such as TET1-3 enzymes, remove methyl groups. The interplay of these components determines the DNA methylation landscape. Disruptions in this balance can lead to altered gene expression, contributing to the development of atherosclerotic lesions. For example, if the 'erasers' are not functioning correctly, hypermethylation can occur, leading to abnormal gene expression and potentially contributing to the progression of Atherosclerosis.

What are the potential future treatments for Atherosclerosis that target DNA methylation, and why is this approach promising?

Promising new therapeutic avenues are emerging that target DNA methylation processes. These interventions aim to stimulate mitochondrial biogenesis, prevent cellular senescence, and restore the epigenetic clock. Targeting DNA methylation is promising because it addresses the underlying molecular mechanisms driving the disease. By modulating these processes, researchers hope to prevent the formation of fatty plaques, slow down the progression of Atherosclerosis, and develop personalized and effective therapies. This approach holds potential for preventing and treating this widespread disease by harnessing the power of epigenetics.