A review on regulation of DNA methylation during post-myocardial infarction

Han, Wenqiang; Wang, Wenxin; Wang, Qinhong; Maduray, Kellina; Hao, Li; Zhong, Jingquan

doi:10.3389/fphar.2024.1267585

Cited by 2 publications

(2 citation statements)

References 229 publications

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“…Furthermore, it has been described that DNMT3a promotes fibroblast activation via the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway in a rat model of cardiac fibrosis and its inhibition has been shown to mitigate the fibrotic disease [67,68]. Like In the failing human heart, fibrosis has been correlated with enhanced DNA methylation [64]. Particularly, CFs exhibit increased DNA methylation status under the ischemic conditions that trigger cardiac fibrosis, which has been associated with an increased expression of DNMT1, DNMT3a, and DNMT3b.…”

Section: Dna Methylationmentioning

confidence: 99%

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Fibroblast Diversity and Epigenetic Regulation in Cardiac Fibrosis

Aguado-Alvaro,

Garitano,

Pelacho

2024

IJMS

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Cardiac fibrosis, a process characterized by excessive extracellular matrix (ECM) deposition, is a common pathological consequence of many cardiovascular diseases (CVDs) normally resulting in organ failure and death. Cardiac fibroblasts (CFs) play an essential role in deleterious cardiac remodeling and dysfunction. In response to injury, quiescent CFs become activated and adopt a collagen-secreting phenotype highly contributing to cardiac fibrosis. In recent years, studies have been focused on the exploration of molecular and cellular mechanisms implicated in the activation process of CFs, which allow the development of novel therapeutic approaches for the treatment of cardiac fibrosis. Transcriptomic analyses using single-cell RNA sequencing (RNA-seq) have helped to elucidate the high cellular diversity and complex intercellular communication networks that CFs establish in the mammalian heart. Furthermore, a significant body of work supports the critical role of epigenetic regulation on the expression of genes involved in the pathogenesis of cardiac fibrosis. The study of epigenetic mechanisms, including DNA methylation, histone modification, and chromatin remodeling, has provided more insights into CF activation and fibrotic processes. Targeting epigenetic regulators, especially DNA methyltransferases (DNMT), histone acetylases (HAT), or histone deacetylases (HDAC), has emerged as a promising approach for the development of novel anti-fibrotic therapies. This review focuses on recent transcriptomic advances regarding CF diversity and molecular and epigenetic mechanisms that modulate the activation process of CFs and their possible clinical applications for the treatment of cardiac fibrosis.

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Section: Dna Methylationmentioning

confidence: 99%

“…In the failing human heart, fibrosis has been correlated with enhanced DNA methylation [ 64 ]. Particularly, CFs exhibit increased DNA methylation status under the ischemic conditions that trigger cardiac fibrosis, which has been associated with an increased expression of DNMT1, DNMT3a, and DNMT3b.…”

Section: Epigenetics In Cardiac Fibrosismentioning

confidence: 99%

Fibroblast Diversity and Epigenetic Regulation in Cardiac Fibrosis

Aguado-Alvaro,

Garitano,

Pelacho

2024

IJMS

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The Influence of Metabolic Risk Factors on the Inflammatory Response Triggered by Myocardial Infarction: Bridging Pathophysiology to Treatment

Ramos-Regalado,

Alcover,

Badimon

et al. 2024

Cells

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Myocardial infarction (MI) sets off a complex inflammatory cascade that is crucial for effective cardiac healing and scar formation. Yet, if this response becomes excessive or uncontrolled, it can lead to cardiovascular complications. This review aims to provide a comprehensive overview of the tightly regulated local inflammatory response triggered in the early post-MI phase involving cardiomyocytes, (myo)fibroblasts, endothelial cells, and infiltrating immune cells. Next, we explore how the bone marrow and extramedullary hematopoiesis (such as in the spleen) contribute to sustaining immune cell supply at a cardiac level. Lastly, we discuss recent findings on how metabolic cardiovascular risk factors, including hypercholesterolemia, hypertriglyceridemia, diabetes, and hypertension, disrupt this immunological response and explore the potential modulatory effects of lifestyle habits and pharmacological interventions. Understanding how different metabolic risk factors influence the inflammatory response triggered by MI and unraveling the underlying molecular and cellular mechanisms may pave the way for developing personalized therapeutic approaches based on the patient’s metabolic profile. Similarly, delving deeper into the impact of lifestyle modifications on the inflammatory response post-MI is crucial. These insights may enable the adoption of more effective strategies to manage post-MI inflammation and improve cardiovascular health outcomes in a holistic manner.

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A review on regulation of DNA methylation during post-myocardial infarction

Cited by 2 publications

References 229 publications

Fibroblast Diversity and Epigenetic Regulation in Cardiac Fibrosis

Fibroblast Diversity and Epigenetic Regulation in Cardiac Fibrosis

The Influence of Metabolic Risk Factors on the Inflammatory Response Triggered by Myocardial Infarction: Bridging Pathophysiology to Treatment

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