Inhibited histone deacetylase 3 ameliorates myocardial ischemia–reperfusion injury in a rat model by elevating <scp>microRNA</scp>‐19a‐3p and reducing cyclin‐dependent kinase 2

Song, Kaiyou; Li, Lianting; Quan, Qingqing; Wei, Yan-Jin; Hu, Shunpeng

doi:10.1002/iub.2402

Cited by 9 publications

(7 citation statements)

References 41 publications

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“…Antioxidant intravitreal injection activated nuclear-factor-E2-related factor 2 (Nrf2) signalling and attenuated retinal dysfunction by light damage in mice, and thus, targeting oxidative stress would be regarded as a therapy for neurodegeneration [ 9 ]. HDAC3 would promote oxidative stress in different diseases, including myocardial ischemia-reperfusion (I/R) injury and spinal cord injury [ 26 , 27 ]. In this study, we demonstrated that HADC3 inhibition could be a potential antioxidative therapy and thus provided us with more knowledge in DR management.…”

Section: Discussionmentioning

confidence: 99%

HDAC3 Inhibition Alleviates High-Glucose-Induced Retinal Ganglion Cell Death through Inhibiting Inflammasome Activation

Tang

Liu

et al. 2022

BioMed Research International

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Purpose. The exact effects of histone deacetylase 3 (HDAC3) inhibition in DR related retinal ganglion cells (RGCs) death remained unclear. This study is aimed at detecting the influence of HDAC3 on the high-glucose-induced retinal ganglion cell death. Methods. The retinal HDAC3 expression in DR of different time points was analyzed by immunohistochemical assay and western blot. Besides, the expression of HDAC3 and both retinal thickness and RGC loss were analyzed. The effects of HDAC3 inhibitor on cell viability, oxidative stress, and apoptosis in high-glucose- (HG-) treated RGCs were analyzed. Both inflammatory and antioxidative factors were detected by ELISA. Results. Advanced effects of HDAC3 inhibition on the expression of NLRP3 inflammasome were detected using western blots. High HDAC3 expression was detected only in the late DR mice (4 months of diabetes duration) but not early DR mice (2 months of diabetes duration). The immunohistochemical assay showed that HDAC3 expression was correlated with both retinal thickness and RCG contents. HDAC3 inhibitor significantly protected the HG-treated RGCs from damaged cell viability, severe apoptosis, and oxidative stress. Advanced pathway analyses showed that HDAC3 inhibition inactivated NLRP3 inflammasome and thus alleviated retinal inflammation. Conclusion. In conclusion, HDAC3 was involved in RGC loss and thus promoted the progression of neurodegeneration of DR. Besides, HDAC3 inhibitor demonstrated protective effects in neurodegeneration in DR through downregulation of NLRP3 activity. The effects of HDAC3 inhibitor in DR management should be confirmed in clinical trials.

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Section: Discussionmentioning

confidence: 99%

HDAC3 Inhibition Alleviates High-Glucose-Induced Retinal Ganglion Cell Death through Inhibiting Inflammasome Activation

Tang

Liu

et al. 2022

BioMed Research International

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“…Cyclin-dependent kinase 2 (CDK2) is a serine/threonine kinase, of which the abnormal activation is related to MI [ 118 ]. RGFP966, a selective inhibitor of HDAC3, can reduce the CDK2 of the myocardium through increasing miR-19a-3p expression, alleviating oxidative stress and even cardiac injury after MI [ 119 ]. Besides cardiomyocytes, the recruitment and phenotypic differentiation of macrophages are also important for myocardial repair and functional remodeling during MI.…”

Section: The Role Of Hdac3 and Its Inhibitors In Chronic Diseasesmentioning

confidence: 99%

The role of HDAC3 and its inhibitors in regulation of oxidative stress and chronic diseases

Liu

Geng

et al. 2023

Cell Death Discov.

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HDAC3 is a specific and crucial member of the HDAC family. It is required for embryonic growth, development, and physiological function. The regulation of oxidative stress is an important factor in intracellular homeostasis and signal transduction. Currently, HDAC3 has been found to regulate several oxidative stress-related processes and molecules dependent on its deacetylase and non-enzymatic activities. In this review, we comprehensively summarize the knowledge of the relationship of HDAC3 with mitochondria function and metabolism, ROS-produced enzymes, antioxidant enzymes, and oxidative stress-associated transcription factors. We also discuss the role of HDAC3 and its inhibitors in some chronic cardiovascular, kidney, and neurodegenerative diseases. Due to the simultaneous existence of enzyme activity and non-enzyme activity, HDAC3 and the development of its selective inhibitors still need further exploration in the future.

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“…It would be interesting to see, if NCoR1 gene silencing could rescue diabetic cardiomyopathy in these mice by inactivating HDAC3 enzymatic activity. Another study found that inhibiting HDAC3 with RGFP966 increased miR-19a-3p and enhanced cardiac function in a rat model of MI/R ( Song et al, 2020 ). In the hearts of rats with streptozotocin (STZ)-induced diabetes, HDAC3 enzymatic activity led to ischemic cardiac damage ( Xie et al, 2014 ; Qiu et al, 2021 ).…”

Section: Heartmentioning

confidence: 99%

Insights into the function of HDAC3 and NCoR1/NCoR2 co-repressor complex in metabolic diseases

Paluvai,

Shanmukha,

Tyedmers

et al. 2023

Front. Mol. Biosci.

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Histone deacetylase 3 (HDAC3) and nuclear receptor co-repressor (NCoR1/2) are epigenetic regulators that play a key role in gene expression and metabolism. HDAC3 is a class I histone deacetylase that functions as a transcriptional co-repressor, modulating gene expression by removing acetyl groups from histones and non-histone proteins. NCoR1, on the other hand, is a transcriptional co-repressor that interacts with nuclear hormone receptors, including peroxisome proliferator-activated receptor gamma (PPARγ) and liver X receptor (LXR), to regulate metabolic gene expression. Recent research has revealed a functional link between HDAC3 and NCoR1 in the regulation of metabolic gene expression. Genetic deletion of HDAC3 in mouse models has been shown to improve glucose intolerance and insulin sensitivity in the liver, skeletal muscle, and adipose tissue. Similarly, genetic deletion of NCoR1 has improved insulin resistance and reduced adiposity in mouse models. Dysregulation of this interaction has been associated with the development of cardio-metabolic diseases such as cardiovascular diseases, obesity and type 2 diabetes, suggesting that targeting this pathway may hold promise for the development of novel therapeutic interventions. In this review, we summarize the current understanding of individual functions of HDAC3 and NCoR1/2 and the co-repressor complex formation (HDAC3/NCoR1/2) in different metabolic tissues. Further studies are needed to thoroughly understand the mechanisms through which HDAC3, and NCoR1/2 govern metabolic processes and the implications for treating metabolic diseases.

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Inhibited histone deacetylase 3 ameliorates myocardial ischemia–reperfusion injury in a rat model by elevating microRNA‐19a‐3p and reducing cyclin‐dependent kinase 2

Cited by 9 publications

References 41 publications

HDAC3 Inhibition Alleviates High-Glucose-Induced Retinal Ganglion Cell Death through Inhibiting Inflammasome Activation

HDAC3 Inhibition Alleviates High-Glucose-Induced Retinal Ganglion Cell Death through Inhibiting Inflammasome Activation

The role of HDAC3 and its inhibitors in regulation of oxidative stress and chronic diseases

Insights into the function of HDAC3 and NCoR1/NCoR2 co-repressor complex in metabolic diseases

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