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October 9, 2025Circulation Research

Abstract Wed016: Loss of β 2 Adrenergic Receptor S-nitrosylation Protects Against Myocardial Injury

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Authors

TRThiele Osvaldt RosalesDuke UniversityHFHeriberto Rodríguez FraustoUniversidad Autónoma de Zacatecas "Francisco García Salinas"RRRajika RoyDuke University

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Implication

In vivo analysis shows β2 adrenergic receptor S-nitrosylation loss reduces myocardial infarct size, suggesting enhanced cardioprotective signaling.

Key Points

  • Mice lacking S-nitrosylation at β2 adrenergic receptors showed reduced infarct size and improved cardiac function after ischemia.
  • Infarct size was significantly lower in β2 AR-C265S KI mice at 32%, compared to 57% in β2 AR WT under identical conditions.
  • Ejection fraction and left ventricular mass were markedly improved in the β2 AR-C265S KI group after reperfusion, supporting enhanced recovery.
  • The preservation of receptor function highlights S-nitrosylation's critical role in cardiac injury response, informing potential new treatments.

Cite This Study

Rosales et al. (2025) studied this question.

synapsesocial.com/papers/68e77f09d1c187e1c108fbb9https://doi.org/10.1161/res.137.suppl_1.wed016
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Also Consider

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  1. 1The denitrosylase SCoR2 controls cardioprotective metabolic reprogramming2025
  2. 2Abstract Wed042: Unveiling the Cardioprotective Role of Sialidase Neu3 in Cardiac Ischemia and Reperfusion Injury2025
  3. 3β-sitosterol ameliorates myocardial infarction injury via modulating the NF-κB and necroptosis signaling pathways2026
  4. 4Effect of probiotic strains, L-arginine and carvedilol on myocardial infarction size in systemic inflammation in rats2025
  5. 5Abstract Wed097: Metabolic Syndrome in Rodents Activates β-adrenergic Receptor Signaling Concealing Defects in Cardiac Performance2025