2018

DOI: 10.1007/s12031-018-1221-0

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HDAC9 Polymorphisms Predict Susceptibility, Severity, and Short-Term Outcome of Large Artery Atherosclerotic Stroke in Chinese Population

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Introduction2

Hdacs In Cerebral Ischemia1

Discussion1

Stroke and Histone Acetylation1

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Cited by 13 publications

(9 citation statements)

References 26 publications

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“…HDAC9 deficiency and downregulation of phosphorylated IkBa are related to the role of phosphorylated nuclear factor-kappa B (NF- κ B) and mitogen-activated protein kinase (MAPKs), including regulating phosphorylated p38, phosphorylated extracellular signal-regulated kinase 1, ERK1/2, and phosphorylated c-Jun n-terminal kinase, in promoting ischemic brain injury [ 42 ]. In addition, HDAC9 polymorphism can be used as a biomarker of susceptibility, severity, and short-term prognosis of atherosclerotic stroke [ 43 ]. However, Su et al [ 44 ] indicate that variant rs2107595 of HDAC9 may have no association with higher ischemic stroke risks in southern Han Chinese.…”

Section: Hdacs In Cerebral Ischemiamentioning

confidence: 99%

Updating a Strategy for Histone Deacetylases and Its Inhibitors in the Potential Treatment of Cerebral Ischemic Stroke

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et al. 2020

Disease Markers

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Background. Cerebral ischemic stroke is one of the severe diseases with a pathological condition that leads to nerve cell dysfunction with seldom available therapy options. Currently, there are few proven effective treatments available for improving cerebral ischemic stroke outcome. However, recently, there is increasing evidence that inhibition of histone deacetylase (HDAC) activity exerts a strong protective effect in in vivo and vitro models of ischemic stroke. Review Summary. HDAC is a posttranslational modification that is negatively regulated by histone acetyltransferase (HATS) and histone deacetylase. Based on function and DNA sequence similarity, histone deacetylases (HDACs) are organized into four different subclasses (I-IV). Modifications of histones play a crucial role in cerebral ischemic affair development after translation by modulating disrupted acetylation homeostasis. HDAC inhibitors (HDACi) mainly exert neuroprotective effects by enhancing histone and nonhistone acetylation levels and enhancing gene expression and protein modification functions. This article reviews HDAC and its inhibitors, hoping to find meaningful therapeutic targets. Conclusions. HDAC may be a new biological target for cerebral ischemic stroke. Future drug development targeting HDAC may make it a potentially effective anticerebral ischemic stroke drug.

“…HDAC9 deficiency and downregulation of phosphorylated IkBa are related to the role of phosphorylated nuclear factor-kappa B (NF- κ B) and mitogen-activated protein kinase (MAPKs), including regulating phosphorylated p38, phosphorylated extracellular signal-regulated kinase 1, ERK1/2, and phosphorylated c-Jun n-terminal kinase, in promoting ischemic brain injury [ 42 ]. In addition, HDAC9 polymorphism can be used as a biomarker of susceptibility, severity, and short-term prognosis of atherosclerotic stroke [ 43 ]. However, Su et al [ 44 ] indicate that variant rs2107595 of HDAC9 may have no association with higher ischemic stroke risks in southern Han Chinese.…”

Section: Hdacs In Cerebral Ischemiamentioning

confidence: 99%

Updating a Strategy for Histone Deacetylases and Its Inhibitors in the Potential Treatment of Cerebral Ischemic Stroke

¹

,

²

,

³

et al. 2020

Disease Markers

View full text Add to dashboard Cite

Background. Cerebral ischemic stroke is one of the severe diseases with a pathological condition that leads to nerve cell dysfunction with seldom available therapy options. Currently, there are few proven effective treatments available for improving cerebral ischemic stroke outcome. However, recently, there is increasing evidence that inhibition of histone deacetylase (HDAC) activity exerts a strong protective effect in in vivo and vitro models of ischemic stroke. Review Summary. HDAC is a posttranslational modification that is negatively regulated by histone acetyltransferase (HATS) and histone deacetylase. Based on function and DNA sequence similarity, histone deacetylases (HDACs) are organized into four different subclasses (I-IV). Modifications of histones play a crucial role in cerebral ischemic affair development after translation by modulating disrupted acetylation homeostasis. HDAC inhibitors (HDACi) mainly exert neuroprotective effects by enhancing histone and nonhistone acetylation levels and enhancing gene expression and protein modification functions. This article reviews HDAC and its inhibitors, hoping to find meaningful therapeutic targets. Conclusions. HDAC may be a new biological target for cerebral ischemic stroke. Future drug development targeting HDAC may make it a potentially effective anticerebral ischemic stroke drug.

“…Previous studies have demonstrated that HDAC9 is associated with the pathogenesis of cardiometabolic diseases such as atherosclerosis [ 13 , 14 , 15 , 16 , 17 ] and diabetes [ 7 ], and that global HDAC9 KO mice are protected against obesity-related metabolic disease. In this study, we investigated the impact of adipocyte-specific HDAC9 gene deletion on metabolic function in HFD-induced obesity using both female and male mice.…”

Section: Discussionmentioning

confidence: 99%

Sex-Dependent Role of Adipose Tissue HDAC9 in Diet-Induced Obesity and Metabolic Dysfunction

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Obesity is a major risk factor for both metabolic and cardiovascular disease. We reported that, in obese male mice, histone deacetylase 9 (HDAC9) is upregulated in adipose tissues, and global deletion of HDAC9 protected against high fat diet (HFD)-induced obesity and metabolic disease. Here, we investigated the impact of adipocyte-specific HDAC9 gene deletion on diet-induced obesity in male and female mice. The HDAC9 gene expression was increased in adipose tissues of obese male and female mice and HDAC9 expression correlated positively with body mass index in humans. Interestingly, female, but not male, adipocyte-specific HDAC9 KO mice on HFD exhibited reduced body weight and visceral adipose tissue mass, adipocyte hypertrophy, and improved insulin sensitivity, glucose tolerance and adipogenic differentiation gene expression. Furthermore, adipocyte-specific HDAC9 gene deletion in female mice improved metabolic health as assessed by whole body energy expenditure, oxygen consumption, and adaptive thermogenesis. Mechanistically, compared to female mice, HFD-fed male mice exhibited preferential HDAC9 expression in the stromovascular fraction, which may have offset the impact of adipocyte-specific HDAC9 gene deletion in male mice. These results suggest that HDAC9 expressed in adipocytes is detrimental to obesity in female mice and provides novel evidence of sex-related differences in HDAC9 cellular expression and contribution to obesity-related metabolic disease.

“…84 HDAC9 expression was increased in the carotid plaques of stroke patients 85 and a single nucleotide polymorphism (SNP) in the HDAC9 gene has been associated with large artery atherosclerotic stroke in multiple stroke patient studies. [85][86][87] This indicates that some individuals carry a genetic susceptibility to stroke via HDAC9-mediated histone acetylation. Furthermore, this suggests that in addition to the critical role of histone acetylation in modulating cerebral ischemic injury (Figure 2), polymorphisms in histone acetylation markers might mediate genetic risk to stroke.…”

Section: Stroke and Histone Acetylationmentioning

confidence: 99%

Epigenetic mechanisms and potential therapeutic targets in stroke

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et al. 2022

J Cereb Blood Flow Metab

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Accumulating evidence indicates a central role for epigenetic modifications in the progression of stroke pathology. These epigenetic mechanisms are involved in complex and dynamic processes that modulate post-stroke gene expression, cellular injury response, motor function, and cognitive ability. Despite decades of research, stroke continues to be classified as a leading cause of death and disability worldwide with limited clinical interventions. Thus, technological advances in the field of epigenetics may provide innovative targets to develop new stroke therapies. This review presents the evidence on the impact of epigenomic readers, writers, and erasers in both ischemic and hemorrhagic stroke pathophysiology. We specifically explore the role of DNA methylation, DNA hydroxymethylation, histone modifications, and epigenomic regulation by long non-coding RNAs in modulating gene expression and functional outcome after stroke. Furthermore, we highlight promising pharmacological approaches and biomarkers in relation to epigenetics for translational therapeutic applications.

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