Nicorandil, a Nitric Oxide Donor and ATP-Sensitive Potassium Channel Opener, Protects Against Dystrophin-Deficient Cardiomyopathy

Afzal, Muhammad Bilal; Reiter, Melanie; Gastonguay, Courtney; McGivern, Jered V.; Guan, Xuan; Ge, Zhi‐Dong; Mack, David L.; Childers, Martin K.; Ebert, Allison D.; Strande, Jennifer L.

doi:10.1177/1074248416636477

Cited by 45 publications

(51 citation statements)

References 59 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…iPSCs as disease models can be used to model intercellular communication between neighboring cell types in the heart by studying the effects of cell‐type–specific exosomes. Numerous studies have validated the use of iPSCs as a model system to study genetic cardiac diseases such as long QT syndrome, LEOPARD syndrome, and Duchenne muscular dystrophy . In addition, there is growing interest in using iPSC‐derived cells to study environmental modifiers of disease.…”

Section: Ipscs As a Tool To Understand Intercellular Communication Inmentioning

confidence: 99%

“…Numerous studies have validated the use of iPSCs as a model system to study genetic cardiac diseases such as long QT syndrome, 27,93 LEOPARD syndrome, 94 and Duchenne muscular dystrophy. 29,95 In addition, there is growing interest in using iPSC-derived cells to study environmental modifiers of disease. The iPSC-derived cells can be exposed to various conditions to precipitate oxidative, metabolic, or endoplasmic reticular stress or subjected to neurohormones, growth factors, or hypoxia to mimic certain disease states.…”

Section: Ipscs As a Tool To Understand Intercellular Communication Inmentioning

confidence: 99%

See 1 more Smart Citation

Examining the Paracrine Effects of Exosomes in Cardiovascular Disease and Repair

Gartz

Strande

2018

JAHA

Self Cite

View full text Add to dashboard Cite

Section: Ipscs As a Tool To Understand Intercellular Communication Inmentioning

confidence: 99%

Section: Ipscs As a Tool To Understand Intercellular Communication Inmentioning

confidence: 99%

Examining the Paracrine Effects of Exosomes in Cardiovascular Disease and Repair

Gartz

Strande

2018

JAHA

Self Cite

View full text Add to dashboard Cite

“…The use of iPSC-CMs to model cardiomyopathic disease has more often been restricted to genetically inherited or spontaneous cardiomyopathies such as hypertrophic cardiomyopathy[43], Pompe’s disease [44], or Duchenne muscular dystrophy [40, 45]. Less commonly, iPSC-CMs are used to model acquired cardiomyopathies such as HFpEF.…”

Section: Patient-specific Ipsc-derived Cardiomyocytes To Study Genetimentioning

confidence: 99%

Molecular Approaches in HFpEF: MicroRNAs and iPSC-Derived Cardiomyocytes

Kriegel

Gartz

Afzal

et al. 2016

J. of Cardiovasc. Trans. Res.

Self Cite

View full text Add to dashboard Cite

Heart failure with preserved left ventricular ejection fraction (HFpEF) has emerged as one of the largest unmet needs in cardiovascular medicine. HFpEF is increasing in prevalence and causes significant morbidity, mortality, and health care resource utilization. Patients have multiple co-morbidities which contribute to the disease complexity. To date, no effective treatment for HFpEF has been identified. The paucity of cardiac biopsies from this patient population and the absence of well-accepted animal models limit our understanding of the underlying molecular mechanisms of HFpEF. In this review, we discuss combining state-of-the-art technologies of microRNA profiling and human induced plu-ripotent cell-derived cardiomyocytes (iPSC-CMs) in order to uncover novel molecular pathways that may contribute to the development of HFpEF. Here, we focus the advantages and limitations of microRNA profiling and iPSC-CMs as a disease model system to discover molecular mechanisms in HFpEF.

show abstract

“…Since then, pharmacological studies showed that KATP openers exerted profound cardioprotective effects in numerous mammalian species (Afzal et al, 2016; Flagg et al, 2010; Gao et al, 2016; Grover & Garlid, 2000; Yamada et al, 2006; Zingman et al, 2002). Following the finding of the mitochondrial KATP that locating at the inner membrane of mitochondria in 1991 (Inoue et al, 1991), Garlid et al (1997) and Liu et al (1998) demonstrated it as a trigger of ischemic preconditioning.…”

Section: Introductionmentioning

confidence: 99%

Ischemic postconditioning and pinacidil suppress calcium overload in anoxia-reoxygenation cardiomyocytes via down-regulation of the calcium-sensing receptor

Zhang

Cao

Deng

et al. 2016

PeerJ

View full text Add to dashboard Cite

Ischemic postconditioning (IPC) and ATP sensitive potassium channel (KATP) agonists (e.g. pinacidil and diazoxide) postconditioning are effective methods to defeat myocardial ischemia-reperfusion (I/R) injury, but their specific mechanisms of reducing I/R injury are not fully understood. We observed an intracellular free calcium ([Ca2+]i) overload in Anoxia/reoxygenation (A/R) cardiomyocytes, which can be reversed by KATP agonists diazoxide or pinacidil. The calcium-sensing receptor (CaSR) regulates intracellular calcium homeostasis. CaSR was reported to be involved in the I/R-induced apoptosis in rat cardiomyocytes. We therefore hypothesize that IPC and pinacidil postconditioning (PPC) reduce calcium overload in I/R cardiomyocytes by the down-regulation of CaSR. A/R model was established with adult rat caridomyocyte. mRNA and protein expression of CaSR were detected, IPC, PPC and KATP’s effects on [Ca2+]i concentration was assayed too. IPC and PPC ameliorated A/R insult induced [Ca2+]i overload in cardiomyocytes. In addition, they down-regulated the mRNA and protein level of CaSR as we expected. CaSR agonist spermine and KATP blocker glibenclamide offset IPC’s effects on CaSR expression and [Ca2+]i modulation. Our data indicate that CaSR down-regulation contributes to the mitigation of calcium overload in A/R cardiomyocytes, which may partially represents IPC and KATP’s myocardial protective mechanism under I/R circumstances.

show abstract

Nicorandil, a Nitric Oxide Donor and ATP-Sensitive Potassium Channel Opener, Protects Against Dystrophin-Deficient Cardiomyopathy

Cited by 45 publications

References 59 publications

Examining the Paracrine Effects of Exosomes in Cardiovascular Disease and Repair

Examining the Paracrine Effects of Exosomes in Cardiovascular Disease and Repair

Molecular Approaches in HFpEF: MicroRNAs and iPSC-Derived Cardiomyocytes

Ischemic postconditioning and pinacidil suppress calcium overload in anoxia-reoxygenation cardiomyocytes via down-regulation of the calcium-sensing receptor

Contact Info

Product

Resources

About