The Role of MKP-1 in Insulin-Induced Cardioprotection

Webster, Ingrid; Smith, A. J.; Lochner, Amanda; Huisamen, Barbara

doi:10.1007/s10557-017-6731-4

Cited by 7 publications

(4 citation statements)

References 12 publications

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“…After screening titles and abstracts, 40 studies were considered potentially eligible for inclusion. After estimating full-text publications, 14 studies were excluded due to intervention or outcome data were unqualified [28][29][30][31][32][33][34][35][36][37][38][39][40][41], and four studies were excluded because pure alkaloids were not assessed [42][43][44][45]. Finally, 22 studies were included in the present meta-analysis [13-14, 19-27, 46-56] (Figure 1).…”

Section: Resultsmentioning

confidence: 99%

Efficacy of Alkaloids in Alleviating Myocardial Ischemia-Reperfusion Injury in Rats: A Meta-Analysis of Animal Studies

Wang

Liu

Zhang

et al. 2021

BioMed Research International

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Background. Animal models are well established for studying the effects of alkaloids in preventing myocardial ischemia-reperfusion injury. However, few studies have investigated the therapeutic effects of alkaloids in humans. This meta-analysis and systematic review assessed the efficacy of alkaloids in attenuating infarct size in rats with myocardial ischemia-reperfusion injury. Methods. An integrated literature search including the PubMed, Embase, and Cochrane Library databases was performed to identify studies that evaluated the therapeutic effects of alkaloids on myocardial ischemia-reperfusion injury in rats. The main outcome was infarct size, and SYRCLE’s risk of bias tool was used to assess the quality of the studies. Results. 22 studies were brought into the meta-analysis. Compared with the effects of vehicle, alkaloids significantly reduced infarct size (standardized mean difference SMD = − 0.45 ; 95% confidence interval CI = − 0.64 to − 0.26 ). In subgroup analyses, isoquinoline alkaloids ( SMD = − 0.43 ; 95 % CI = − 0.70 to − 0.16 ) significantly reduced infarct size versus the control. Conclusion. Isoquinoline alkaloids can potentially alleviate myocardial ischemia-reperfusion injury. This meta-analysis and systematic review supply a reference for research programs aiming to develop alkaloid-based clinical drugs. This trial is registered with CRD42019135489.

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Section: Resultsmentioning

confidence: 99%

Efficacy of Alkaloids in Alleviating Myocardial Ischemia-Reperfusion Injury in Rats: A Meta-Analysis of Animal Studies

Wang

Liu

Zhang

et al. 2021

BioMed Research International

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“…1E). Of note, GO and KEGG analyses predicted that MAPK phosphatase activity and the inhibition of MKP-1 mRNA expression might exert a cardioprotective effect in the ischemic rat model (Webster et al, 2017;Yoshikawa et al, 2019).…”

Section: Downregulation Of Mkp-1 Gene Expression In Rat Ischemic Hear...mentioning

confidence: 99%

Dexmedetomidine alleviates oxygen and glucose deprivation-induced apoptosis in mesenchymal stem cell via downregulation of MKP-1

GUAN¹,

ZENG²,

GAO³

et al. 2022

Biocell

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Bone marrow mesenchymal stem cell (MSC)-based therapy is a novel candidate for heart repair. But ischemiareperfusion injury leads to low viability of MSC. Dexmedetomidine (Dex) has been found to protect neurons against ischemia-reperfusion injury. It remains unknown if Dex could increase the viability of MSCs under ischemia. The present study is to observe the potential protective effect of Dex on MSCs under ischemia and its underlying mechanisms. Specific mRNAs related to myocardial ischemia in the GEO database were selected from the mRNA profiles assessed in a previous study using microarray. The most dysregulated mRNAs of the specific ones from the above study were subject to bioinformatics analysis at our laboratory. These dysregulated mRNAs possibly regulated apoptosis of cardiomyocytes and were validated in vitro for their protective effect on MSCs under ischemia. MSCs were pre-treated with Dex at 10 μM concentration for 24 h under oxygen-glucose deprivation (OGD). Flow cytometry and TUNEL assay were carried out to detect apoptosis in Dex-pretreated MSCs under OGD. The relative expressions of mitogen-activated protein kinase phosphatase 1 (MKP-1) and related genes were detected by quantitative polymerase chain reaction and western blotting. Microarray data analysis revealed that Dex regulates MAPK phosphatase activity. Dex significantly reduced in vitro apoptosis of MSCs under OGD, which suppressed the synthesis level of Beclin1 and light chain 3 proteins. Dex down-regulated MKP-1 expression and attenuated an OGDinduced change in the mitogen activated protein kinase 3 (MAPK3) signaling pathway. Dex increases the viability of MSC and improves its tolerance to OGD in association with the MKP-1 signaling pathway, thus suggesting the potential of Dex as a novel strategy for promoting MSCs efficacy under ischemia.

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“…Reperfusion is critical in rescuing the ischemic myocardium from infarction and cardiomyocyte death [43,44]. Insulin protects cardiac myocytes [45,46] while oxidative stress [44] has been implicated in ischemia-reperfusion induced cardiomyocyte apoptosis [44]. In cardiac myocytes, insulin resistance affects the cytoprotective effects of insulin that is mediated by induction of MKP-1 expression [47].…”

Section: Mkp-1 In Cardioprotectionmentioning

confidence: 99%

“…Considering the fact that studies on cardioprotective effects of MKP-1 [45,[47][48][49] including stress-responsive MAPK [68] are controversial, more studies are needed to elucidate how modulation of MKP-1 could be beneficial in the treatment of cardiac diseases. Future work will require cardioprotective analysis of MKP-1 in tissue-specific mouse models.…”

Section: Inhibition Of Mkp-1 In Musclementioning

confidence: 99%

Improving Obesity and Insulin Resistance by Targeting Skeletal Muscle MKP-1

Bennett

Lawan

2020

Journal of Cellular Signaling

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Obesity has reached a global epidemic and it predisposes to the development of insulin resistance, type 2 diabetes and related metabolic diseases. Current interventions against obesity and/or type 2 diabetes such as calorie restriction, exercise, genetic manipulations or established pharmacological treatments have not been successful for many patients with obesity and/or type 2 diabetes. There is an urgent need for new strategies to treat insulin resistance, T2D and obesity. Increased activity of stress-responsive pathways has been linked to the pathogenesis of insulin resistance in obesity. In this commentary, we argue that chronic upregulation of MKP-1 in skeletal muscle is part of a stress response that contributes to the development of insulin resistance, T2D and obesity. Therefore, inhibition of MKP-1 in skeletal muscle is a potential strategy for the treatment of T2D and obesity. We highlight therapeutic strategies for potential targeting of MKP-1 in skeletal muscle for the treatment of metabolic diseases as well as other diseases of skeletal muscle.

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The Role of MKP-1 in Insulin-Induced Cardioprotection

Cited by 7 publications

References 12 publications

Efficacy of Alkaloids in Alleviating Myocardial Ischemia-Reperfusion Injury in Rats: A Meta-Analysis of Animal Studies

Efficacy of Alkaloids in Alleviating Myocardial Ischemia-Reperfusion Injury in Rats: A Meta-Analysis of Animal Studies

Dexmedetomidine alleviates oxygen and glucose deprivation-induced apoptosis in mesenchymal stem cell via downregulation of MKP-1

Improving Obesity and Insulin Resistance by Targeting Skeletal Muscle MKP-1

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