QGC606: A Best-in-Class Orally Active Centrally Acting Aminopeptidase A Inhibitor Prodrug for Treating Heart Failure Following Myocardial Infarction

Boitard, Solene; Keck, Mathilde; Deloux, Robin; Girault-Sotias, Pierre-Emmanuel; Marc, Yannick; Mota, Nadia De; Compère, Delphine; Agbulut, Onnik; Balavoine, Fabrice; Llorens-Cortes, Catherine

doi:10.1016/j.cjca.2022.01.019

Cited by 4 publications

(1 citation statement)

References 42 publications

(65 reference statements)

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“…Moreover, eplerenone, a well-tolerated selective MRA, decreases PIIINP with good efficacy when baseline PIIINP is ≥3.6 mmol/L after MI with HF or diabetes ( Stienen et al, 2020 ). As a centrally acting aminopeptidase A inhibitor prodrug, QGC606 inhibits the overactivation of the brain renin-angiotensin system and fibrotic remodeling without lowering blood pressure ( Boitard et al, 2022 ).…”

Section: Interventions For Cardiac Fibrosismentioning

confidence: 99%

Post-myocardial infarction fibrosis: Pathophysiology, examination, and intervention

Yin

Pan

et al. 2023

Front. Pharmacol.

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Cardiac fibrosis plays an indispensable role in cardiac tissue homeostasis and repair after myocardial infarction (MI). The cardiac fibroblast-to-myofibroblast differentiation and extracellular matrix collagen deposition are the hallmarks of cardiac fibrosis, which are modulated by multiple signaling pathways and various types of cells in time-dependent manners. Our understanding of the development of cardiac fibrosis after MI has evolved in basic and clinical researches, and the regulation of fibrotic remodeling may facilitate novel diagnostic and therapeutic strategies, and finally improve outcomes. Here, we aim to elaborate pathophysiology, examination and intervention of cardiac fibrosis after MI.

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Section: Interventions For Cardiac Fibrosismentioning

confidence: 99%