The nuclear receptor co-repressor 1 is a novel cardioprotective factor against acute myocardial ischemia-reperfusion injury

Qin, Zihan; Gao, Liang; Lin, Guanqiao; Zhu, Hong; Chen, Yingmin; Zhong, Fangyuan; Zhou, Hongmei; Duan, Sheng-Zhong; Pu, Jun

doi:10.1016/j.yjmcc.2022.01.006

Cited by 7 publications

(3 citation statements)

References 50 publications

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“…Moreover, epigenomic and transcriptomic analysis data identified STAT1 as a direct transcriptional repressor target of NCoR1. This demonstrates that cardiomyocyte-expressed NCoR1 functions as a crucial cardioprotective factor against acute MI/RI by targeting the STAT1 pathway in the heart ( Qin et al, 2022 ). See Figure 5 .…”

Section: Review Of Potential Mechanisms Of Tsi On Mi/rimentioning

confidence: 99%

Network pharmacology-based analysis of potential mechanisms of myocardial ischemia-reperfusion injury by total salvianolic acid injection

Li,

Gu,

Liu

et al. 2023

Front. Pharmacol.

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In this review, we investigated the potential mechanism of Total Salvianolic Acid Injection (TSI) in protecting against myocardial ischemia reperfusion injury (MI/RI). To achieve this, we predicted the component targets of TSI using Pharmmapper and identified the disease targets of MI/RI through GeneCards, DisGenNET, and OMIM databases. We constructed protein-protein interaction networks by analyzing the overlapping targets and performed functional enrichment analyses using Gene Ontology and Kyoto Encyclopedia of Genes and Genomes. Our analysis yielded 90 targets, which were implicated in the potential therapeutic effects of TSI on MI/RI. Seven critical signaling pathways significantly contributed to TSI’s protective effects, namely, PI3K signaling, JAK-STAT signaling, Calcium signaling, HIF-1 signaling, Nuclear receptor signaling, Cell Cycle, and Apoptosis. Subsequently, we conducted a comprehensive literature review of these seven key signaling pathways to gain further insights into their role in the TSI-mediated treatment of MI/RI. By establishing these connections, our study lays a solid foundation for future research endeavours to elucidate the molecular mechanisms through which TSI exerts its beneficial effects on MI/RI.

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Section: Review Of Potential Mechanisms Of Tsi On Mi/rimentioning

confidence: 99%

Network pharmacology-based analysis of potential mechanisms of myocardial ischemia-reperfusion injury by total salvianolic acid injection

Li,

Gu,

Liu

et al. 2023

Front. Pharmacol.

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“…NCoR1 deficiency led to cardiac hypertrophy under physiological conditions and worsened hypertrophy induced by pressure overload ( Li et al, 2019 ), suggesting NCoR1 may be considered as a stress-responsive and cardioprotective regulator during cardiac hypertrophy ( Li et al, 2019 ). NCoR1 was shown to be highly expressed in the mouse heart and to be significantly downregulated after acute myocardial ischemia-reperfusion (MI/R) injury by activation of STAT1 (Janus Kinase/Signal Transducer and Activator of Transcription) pathway ( Qin et al, 2022 ). Pro-inflammatory cytokines such as interferons can activate the JAK/STAT1 pathway following MI/R damage.…”

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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“…Nevertheless, reperfusion can cause secondary myocardial injury in the patients undergoing PCI therapy (5). This sudden myocardial reperfusion after ischemia can induce a series of pathological processes, such as oxidative stress, Ca 2+ overload, altered mitochondrial function, DNA strand breaks, and cell damages, which is termed as ischemia-reperfusion injury (IRI) (6)(7)(8). Prolonged myocardial IRI may further develop cardiac remodeling and even heart failure, which severely influences clinical prognosis (9).…”

Section: Introductionmentioning

confidence: 99%

PPARγ Mediates the Cardioprotective Roles of Danlou Tablet After Acute Myocardial Ischemia-Reperfusion Injury

Meng

Guo

Meng

et al. 2022

Front. Cardiovasc. Med.

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Ischemic heart disease is one of the biggest threats to human life in the world. Reperfusion therapy is an effective strategy to reduce infarct size and ischemic injury. However, reperfusion process may cause secondary myocardial injury which is defined as ischemia-reperfusion injury (IRI). Exploring potential therapeutic strategy to attenuate IRI is extremely important. Danlou tablet (Dan), a Chinese herbal compound consisting of ten herbs, has been identified to be protective for the heart. However, the mechanism of Dan-induced cardioprotection after acute reperfusion was unelucidated. In this study, to investigate the role and mechanism of Dan in myocardial IRI, we performed acute IRI modeling in mice and oxygen-glucose deprivation–reperfusion (OGD/R)-induced apoptosis in primary neonatal rat cardiomyocytes (NRCMs). We found that Dan had protective effect against acute IRI in mice, as evidenced by reduced infarct size, TUNEL-positive cardiomyocytes (CMs), and Bax/Bcl2 ratio and cleaved-caspase 3/caspase 3 ratio in vivo. Meanwhile, Dan inhibited OGD/R-induced apoptosis of NRCMs in vitro. Mechanistically, Dan could activate proliferator-activated receptor gamma (PPARγ) in both IRI hearts and OGD/R-stressed NRCMs, while inhibition of PPARγ attenuated the protective effect of Dan against IRI in vivo and OGD/R-induced CM apoptosis in vitro. These data reveal that Dan attenuates acute myocardial IRI and CM apoptosis through activating PPARγ. Our findings may extend the knowledge of Chinese medicine and provide potential strategy for the precise treatment of ischemic heart diseases.

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The nuclear receptor co-repressor 1 is a novel cardioprotective factor against acute myocardial ischemia-reperfusion injury

Cited by 7 publications

References 50 publications

Network pharmacology-based analysis of potential mechanisms of myocardial ischemia-reperfusion injury by total salvianolic acid injection

Network pharmacology-based analysis of potential mechanisms of myocardial ischemia-reperfusion injury by total salvianolic acid injection

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

PPARγ Mediates the Cardioprotective Roles of Danlou Tablet After Acute Myocardial Ischemia-Reperfusion Injury

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