New Insight in HDACs: Potential Therapeutic Targets for the Treatment of Atherosclerosis

Abstract

Atherosclerosis (AS) features include progressive hardening and reduced elasticity of arteries. AS is the leading cause of morbidity and mortality. An increasing amount of evidence showed that epigenetic modifications on genes serve are a main cause of several diseases, including AS. Histone deacetylases (HDACs) promote the deacetylation at lysine residues, thereby condensing the chromatin structures and further inhibiting the transcription of downstream genes. HDACs widely affect various physiological and pathological processes through transcriptional regulation or deacetylation of other non-histone proteins. In recent years, the role of HDACs in vascular systems has been revealed, and their effects on atherosclerosis have been widely reported. In this review, we discuss the members of HDACs in vascular systems, determine the diverse roles of HDACs in AS, and reveal the effects of HDAC inhibitors on AS progression. We provide new insights into the potential of HDAC inhibitors as drugs for AS treatment.

Paeonol inhibits chronic constriction injury‐induced astrocytic activation and neuroinflammation in rats via the HDAC/miR‐15a pathway

“…Emerging research works have demonstrated that astrocyte was the major regulator of neurotransmitter homeostasis, and activated astrocyte was associated with neuroinflammation in the pathological process of NP (Lee et al, 2018). In the present study, both real-time Histone deacetylases (HDACs) are key regulators in epigenetic modifications and restrain gene expression in multiple diseases by medicating the interactions between histones and transcription factors (Luan et al, 2022). Several studies have found that HDAC1, HDAC2, HDAC4, HDAC5, SIRT1, and SIRT2 were involved in NP (Lin et al, 2015;Miao et al, 2020;Penas & Navarro, 2018).…”

“…Histone deacetylases (HDACs) are key regulators in epigenetic modifications and restrain gene expression in multiple diseases by medicating the interactions between histones and transcription factors (Luan et al, 2022). Several studies have found that HDAC1, HDAC2, HDAC4, HDAC5, SIRT1, and SIRT2 were involved in NP (Lin et al, 2015; Miao et al, 2020; Penas & Navarro, 2018).…”

PRC2-dependent regulation of ganglioside expression during dedifferentiation contributes to the proliferation and migration of vascular smooth muscle cells

“…Therefore, although the involvement of these components in ganglioside synthesis in VSMCs is speculated, it is required to clarify their contribution in the future. Accumulating evidence suggests a critical role for HDACs in regulating vascular cell homeostasis and atherosclerosis ( Chen et al, 2020 ; Luan et al, 2022 ). Sun et al ( Sun et al, 2020 ) reported that HDAC1 is critical for the migration and phenotypic switching of aortic VSMCs.…”

Cardiac cell senescence: molecular mechanisms, key proteins and therapeutic targets

“…Histone acetyltransferases loosen the nucleosome by transferring the acetyl group to histones to facilitate gene transcription. Conversely, histone acetyltransferases remove the acetyl group, promoting histone-DNA interactions and increasing nucleosome compaction [ 174 ]. Histone deacetylases are classified into four groups, and their activities depend on either zinc or NAD + .…”