Life sciences · 2025
The σ1 receptor is a target for the development of cardioprotective drugs.
СтатьяОбзорНазвание и аннотация: Перевод в очереди
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Maslov Leonid N, Tsirulnikov Kirill, Slidnevskaya Alisa S, Kilin Mikhail, Kan Artur, Grab Alexandr E, Gorbunov Alexandr S, Singh Nirmal
Аннотация
BACKGROUND: In-hospital mortality in patients with acute myocardial infarction (AMI) is 4.6 % - 7.5 %. One of the causes of death is reperfusion cardiac injury (RCI). The most common cause of death in AMI is cardiogenic shock. Studying the cardiovascular effects of σ1-receptor agonists can contribute to the development of drugs for the treatment of RCI.
METHODS: A search for relevant topical articles was performed using the PubMed database.
FINDINGS: The σ1-receptor is expressed in cardiomyocytes and endothelial cells. The σ1-receptor was found in the cell membrane, the endoplasmic reticulum (ER), and mitochondria. It is coupled to the inositol triphosphate (IP3) receptor and ryanodine receptors in the ER. The σ1-receptor regulates Ca2+ transport in the ER and mitochondria. σ1-Receptor agonists increase contractility of isolated cardiomyocytes and the heart in vivo. Chronic activation of the σ1-receptor mitigates the development of pressure overload-induced adverse remodeling of the heart. Activation of the σ1-receptor inhibits apoptosis of cardiomyocytes in ischemia/reperfusion of the heart. σ1-Receptor stimulation promotes the activation of protein kinase C, Akt, NO-synthase, and heme oxygenase-1. Stimulation of σ1-receptor contributes to the closure of mitochondrial permeability pore. Presumably mitochondria are responsible for effects of σ1-receptor agonists.
CONCLUSION: σ1-Receptor agonists may become the basis for the development of drugs for the treatment of AMI and cardiogenic shock and the prevention of adverse cardiac remodeling.
METHODS: A search for relevant topical articles was performed using the PubMed database.
FINDINGS: The σ1-receptor is expressed in cardiomyocytes and endothelial cells. The σ1-receptor was found in the cell membrane, the endoplasmic reticulum (ER), and mitochondria. It is coupled to the inositol triphosphate (IP3) receptor and ryanodine receptors in the ER. The σ1-receptor regulates Ca2+ transport in the ER and mitochondria. σ1-Receptor agonists increase contractility of isolated cardiomyocytes and the heart in vivo. Chronic activation of the σ1-receptor mitigates the development of pressure overload-induced adverse remodeling of the heart. Activation of the σ1-receptor inhibits apoptosis of cardiomyocytes in ischemia/reperfusion of the heart. σ1-Receptor stimulation promotes the activation of protein kinase C, Akt, NO-synthase, and heme oxygenase-1. Stimulation of σ1-receptor contributes to the closure of mitochondrial permeability pore. Presumably mitochondria are responsible for effects of σ1-receptor agonists.
CONCLUSION: σ1-Receptor agonists may become the basis for the development of drugs for the treatment of AMI and cardiogenic shock and the prevention of adverse cardiac remodeling.