Stimulation of Erythrocyte Soluble Guanylyl Cyclase Induces cGMP Export and Cardioprotection in Type 2 Diabetes

Reduced nitric oxide (NO) bioactivity in red blood cells (RBCs) is critical for augmented myocardial ischemia-reperfusion injury in type 2 diabetes. This study identified the nature of “NO bioactivity” by stimulating the intracellular NO receptor soluble guanylyl cyclase (sGC) in RBCs. sGC stimulati...

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Detalles Bibliográficos
Autores principales: Jiao, Tong, Collado, Aida, Mahdi, Ali, Tengbom, John, Tratsiakovich, Yahor, Milne, G. Todd, Alvarsson, Michael, Lundberg, Jon O., Zhou, Zhichao, Yang, Jiangning, Pernow, John
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2023
Materias:
Original Research - Clinical
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10504399/
https://www.ncbi.nlm.nih.gov/pubmed/37719424
http://dx.doi.org/10.1016/j.jacbts.2023.02.017
Descripción
Sumario:Reduced nitric oxide (NO) bioactivity in red blood cells (RBCs) is critical for augmented myocardial ischemia-reperfusion injury in type 2 diabetes. This study identified the nature of “NO bioactivity” by stimulating the intracellular NO receptor soluble guanylyl cyclase (sGC) in RBCs. sGC stimulation in RBCs from patients with type 2 diabetes increased export of cyclic guanosine monophosphate from RBCs and activated cardiac protein kinase G, thereby attenuating ischemia-reperfusion injury. These results provide novel insight into RBC signaling by identifying cyclic guanosine monophosphate from RBC as a mediator of protection against cardiac ischemia-reperfusion injury induced by sGC stimulation in RBCs.

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