Targeting Epigenetic Mechanisms in Vascular Aging

Abstract

Environment, diseases, lack of exercise, and aged tendency of population have becoming crucial factors that induce vascular aging. Vascular aging is unmodifiable risk factor for diseases like diabetes, hypertension, atherosclerosis, and hyperlipidemia. Effective interventions to combat this vascular function decline is becoming increasingly urgent as the rising hospitalization rate caused by vascular aging-related diseases. Fortunately, recent transformative omics approaches have enabled us to examine vascular aging mechanisms at unprecedented levels and precision, which make our understanding of slowing down or reversing vascular aging become possible. Epigenetic viz. DNA methylation, histone modifications, and non-coding RNA-based mechanisms, is a hallmark of vascular aging, its deregulation leads to aberrant transcription changes in tissues. Epigenetics mechanisms by mediating covalent modifications to DNA and histone proteins, consequently, influence the sensitivity and activities of signaling pathways in cells and tissues. A growing body of evidence supports correlations between epigenetic changes and vascular aging. In this article, we will provide a comprehensive overview of epigenetic changes associated with vascular aging based on the recent findings with a focus on molecular mechanisms of action, strategies to reverse epigenetic changes, and future perspectives.

Clonal hematopoiesis and cardiovascular disease: deciphering interconnections

“…A potential mediator in this respect is Beclin-1, which is central to the assembly of autophagosomes and the expression of which is controlled by TET2-dependent de-methylation of promotor sequences [ 72 ]. It is worth noting in this context that changes in DNA methylation-patterns have widely been associated with increased atherosclerotic risk [ 6 , 63 , 73 ].…”

HDAC4 Inhibitors as Antivascular Senescence Therapeutics

“…Vascular injury or damage accumulated in vascular senescence also results in vascular endothelial cell proliferation and migration, causing hypertrophic growth [ 46 ]. Vascular inflammation is observed in the two situations [ 47 ]. In the first, Smyd3 (SET and MYND domain-containing protein 3), a methyltransferase inducing trimethylation of lysine 4 on histone 3 (H3K4me3), participates in Ang II-induced vascular senescence.…”

Discovery of deoxyandrographolide and its novel effect on vascular senescence by targeting HDAC1

“…Vascular senescence (VS) is a complex biological process (BP) that leads to vessel dysfunction and abnormal vascular morphology. 1,2 There is no simple approach to understanding the whole process of VS, 3 and thus preventing VS-related diseases requires long-term attention and constant interventions. VS occurs particularly in elderly people, and its related cardiovascular diseases, such as hypertension, diabetes, and atherosclerotic disease, have become a serious global health event and public burden.…”

“…Vascular senescence (VS) is a complex biological process (BP) that leads to vessel dysfunction and abnormal vascular morphology 1,2 . There is no simple approach to understanding the whole process of VS, 3 and thus preventing VS‐related diseases requires long‐term attention and constant interventions.…”