Impact of pharmacists during in-hospital resuscitation or medical emergency response events: A systematic review

Currey, Elizabeth M.; Falconer, Nazanin; Isoardi, Katherine Z.; Barras, Michael

doi:10.1016/j.ajem.2023.10.020

Cited by 6 publications

(1 citation statement)

References 71 publications

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“…Despite the achievements of modern cardiology, mortality in patients with acute myocardial infarction (AMI) remains high [1][2][3][4][5]. Mortality is especially high in patients with large infarct size, microvascular obstruction, and cardiogenic shock [6][7][8].…”

Section: Introductionmentioning

confidence: 99%

Peptides Are Cardioprotective Drugs of the Future: The Receptor and Signaling Mechanisms of the Cardioprotective Effect of Glucagon-like Peptide-1 Receptor Agonists

Boshchenko,

Maslov,

Mukhomedzyanov

et al. 2024

IJMS

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The high mortality rate among patients with acute myocardial infarction (AMI) is one of the main problems of modern cardiology. It is quite obvious that there is an urgent need to create more effective drugs for the treatment of AMI than those currently used in the clinic. Such drugs could be enzyme-resistant peptide analogs of glucagon-like peptide-1 (GLP-1). GLP-1 receptor (GLP1R) agonists can prevent ischemia/reperfusion (I/R) cardiac injury. In addition, chronic administration of GLP1R agonists can alleviate the development of adverse cardiac remodeling in myocardial infarction, hypertension, and diabetes mellitus. GLP1R agonists can protect the heart against oxidative stress and reduce proinflammatory cytokine (IL-1β, TNF-α, IL-6, and MCP-1) expression in the myocardium. GLP1R stimulation inhibits apoptosis, necroptosis, pyroptosis, and ferroptosis of cardiomyocytes. The activation of the GLP1R augments autophagy and mitophagy in the myocardium. GLP1R agonists downregulate reactive species generation through the activation of Epac and the GLP1R/PI3K/Akt/survivin pathway. The GLP1R, kinases (PKCε, PKA, Akt, AMPK, PI3K, ERK1/2, mTOR, GSK-3β, PKG, MEK1/2, and MKK3), enzymes (HO-1 and eNOS), transcription factors (STAT3, CREB, Nrf2, and FoxO3), KATP channel opening, and MPT pore closing are involved in the cardioprotective effect of GLP1R agonists.

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