Key result
Therapeutics targeting cGMP signaling show promise for HF by inhibiting detrimental myocardial cAMP responses.
Why the study?
Most approved heart failure drugs target HFrEF, but molecules participating in cGMP signaling inhibit detrimental cAMP-mediated responses, making them promising targets for novel therapeutics.
Molecules participating in cGMP signaling are promising targets for novel heart failure therapies, as cGMP signaling inhibits detrimental cAMP-mediated responses in the myocardium.
Current drugs for treating heart failure (HF), for example, angiotensin II receptor blockers and β-blockers, possess specific target molecules involved in the regulation of the cardiac circulatory system. However, most clinically approved drugs are effective in the treatment of HF with reduced ejection fraction (HFrEF). Novel drug classes, including angiotensin receptor blocker/neprilysin inhibitor (ARNI), sodium-glucose co-transporter-2 (SGLT2) inhibitor, hyperpolarization-activated cyclic nucleotide-gated (HCN) channel blocker, soluble guanylyl cyclase (sGC) stimulator/activator, and cardiac myosin activator, have recently been introduced for HF intervention based on their proposed novel mechanisms. SGLT2 inhibitors have been shown to be effective not only for HFrEF but also for HF with preserved ejection fraction (HFpEF). In the myocardium, excess cyclic adenosine monophosphate (cAMP) stimulation has detrimental effects on HFrEF, whereas cyclic guanosine monophosphate (cGMP) signaling inhibits cAMP-mediated responses. Thus, molecules participating in cGMP signaling are promising targets of novel drugs for HF. In this review, we summarize molecular pathways of cGMP signaling and clinical trials of emerging drug classes targeting cGMP signaling in the treatment of HF.
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Mangmool et al. (2023) conducted a review in Heart failure. Therapeutics targeting cGMP signaling was evaluated. Therapeutics targeting cGMP signaling represent promising novel interventions for heart failure by inhibiting detrimental cAMP-mediated responses in the myocardium.
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