GO:0016941 natriuretic peptide receptor activity: Mechanism, Genes and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0016941 natriuretic peptide receptor activity is a molecular function defined as combining with a natriuretic peptide and transmitting the signal to initiate a change in cell activity.
• The principal receptors are NPR1 (NPR-A), NPR2 (NPR-B) and NPR3 (NPR-C), which bind atrial, B-type and C-type natriuretic peptides.
• Ligand binding to NPR-A or NPR-B activates a transmembrane guanylyl cyclase domain that produces cyclic GMP, a central second messenger in cardiovascular and skeletal biology.
• Natriuretic peptide receptor signalling is a validated therapeutic axis in heart failure, pulmonary arterial hypertension and atrial fibrillation.
• CRISPR knockout, point-mutation, knock-in and overexpression cell models allow causal dissection of NPR-A, NPR-B and NPR-C signalling in disease-relevant backgrounds.
• GO:0016941 is best studied with receptor-binding assays, cGMP quantification, phosphoproteomics and CRISPR-engineered isogenic cell lines.
Description
GO:0016941 natriuretic peptide receptor activity is a Gene Ontology molecular function that describes the ability of a receptor to combine with a natriuretic peptide and transmit the signal to initiate a change in cell activity. Natriuretic peptides are a family of hormones that include atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP) and C-type natriuretic peptide (CNP), and they act as central regulators of blood volume, vascular tone and cardiac remodelling. The receptors that carry this activity are the membrane guanylyl cyclases NPR-A (gene NPR1), NPR-B (gene NPR2) and the clearance receptor NPR-C (gene NPR3), which together define the natriuretic peptide axis. Because this activity converts an extracellular peptide signal into intracellular cyclic GMP, it is a direct molecular entry point for understanding cardiovascular homeostasis and for designing therapeutics. For researchers, GO:0016941 is important because it links ligand recognition to a measurable enzymatic output, making it tractable for genetic and pharmacological perturbation. Loss- or gain-of-function studies of NPR1, NPR2 and NPR3 have clarified how natriuretic peptide signalling controls cardiac load, atrial electrophysiology and vascular remodelling. The pathway is also druggable: angiotensin receptor-neprilysin inhibitors raise natriuretic peptide availability, and soluble guanylate cyclase stimulators such as riociguat act downstream of receptor activation. Consequently, GO:0016941 sits at the intersection of endocrinology, cardiology and molecular pharmacology, and it is a frequent target for CRISPR-based functional genomics. This article summarises the authoritative definition, the receptor proteins that execute this activity, the signalling steps they trigger, the human diseases linked to the pathway, and the experimental models and methods used to study it. All statements are anchored to published literature so that the content can support both search retrieval and generative-AI summarisation.
natriuretic peptide receptor activity At A Glance
| GO ID | GO:0016941 |
|---|---|
| GO term | natriuretic peptide receptor activity |
| Ontology | molecular_function |
| Synonym | none |
| Definition | Combining with a natriuretic peptide and transmitting the signal to initiate a change in cell activity. |
| Major function | Ligand-activated signal transduction that converts natriuretic peptide binding into intracellular cyclic GMP signalling. |
| Primary receptors | NPR-A (NPR1), NPR-B (NPR2) and NPR-C (NPR3). |
| Principal ligands | ANP, BNP and CNP, with receptor selectivity determined by the ligand and receptor ectodomain. |
| Second messenger | Cyclic GMP produced by the guanylyl cyclase domain of NPR-A and NPR-B. |
| Therapeutic relevance | Targeted by angiotensin receptor-neprilysin inhibitors and soluble guanylate cyclase stimulators in cardiovascular disease. |
What Is GO:0016941?
In practical terms, GO:0016941 natriuretic peptide receptor activity means that a receptor protein binds a natriuretic peptide ligand and, upon binding, transmits a signal that changes what the cell does. The QuickGO definition states that this activity involves combining with a natriuretic peptide and transmitting the signal to initiate a change in cell activity. This distinguishes the term from simple peptide binding: the receptor must not only bind the hormone but also propagate the signal. In the canonical case, the signal is propagated by a guanylyl cyclase catalytic domain that generates cyclic GMP, which then acts on downstream effectors. The term is therefore a molecular function annotation that captures both recognition and signal transduction, and it is assigned to receptors such as NPR-A and NPR-B that mediate natriuretic peptide responses.
Why Is natriuretic peptide receptor activity Important in Cell Biology?
GO:0016941 is important because it defines the molecular step at which natriuretic peptides exert their endocrine and paracrine effects, and this step is directly implicated in heart failure, pulmonary arterial hypertension, atrial fibrillation and vascular disease. Because the activity is enzymatic and measurable, it provides a clean readout for genetic perturbation, and because the receptors are cell-surface proteins, they are accessible to therapeutic antibodies, peptides and small molecules. Understanding this activity therefore supports both mechanistic biology and translational drug development.
• Defines the receptor function that converts natriuretic peptide binding into intracellular cyclic GMP signalling.
• Controls blood volume, vascular tone and cardiac remodelling through NPR-A and NPR-B activation.
• NPR-B signalling in the atrium regulates cyclic AMP and protects against atrial fibrillation.
• NPR-A and NPR-B augmentation is being pursued as a therapeutic strategy in heart failure.
• NPR-C acts as a clearance receptor that modulates local natriuretic peptide availability.
• The pathway is pharmacologically tractable, as shown by neprilysin inhibition and guanylate cyclase stimulation.
• Engineered natriuretic peptide analogues such as CRRL269 illustrate receptor-selective drug design.
• GO:0016941 provides a functional annotation for interpreting cardiovascular and skeletal phenotypes in genetic screens.
• The activity is a useful endpoint in CRISPR knockout and knock-in studies of NPR1, NPR2 and NPR3.
• It connects hormone biology to cyclic GMP-dependent processes in multiple tissues.
Core Biology of GO:0016941 natriuretic peptide receptor activity
Ligand recognition and receptor binding
In simple terms: The receptor first has to grab the hormone, like a lock accepting the right key.
Natriuretic peptide receptor activity begins with selective binding of a natriuretic peptide to the receptor ectodomain. ANP and BNP preferentially engage NPR-A, whereas CNP preferentially engages NPR-B, and NPR-C binds all three peptides with high affinity as a clearance receptor. Structural analysis of hormone recognition by NPR-A has clarified how the receptor ectodomain discriminates among natriuretic peptides, providing a molecular basis for receptor selectivity. This binding step is the defining event of GO:0016941 because it is the point at which the receptor combines with its peptide ligand.
Receptor activation and guanylyl cyclase stimulation
In simple terms: Once the hormone is bound, the receptor switches on an enzyme that makes a signalling molecule.
Ligand binding to NPR-A or NPR-B activates the receptor's intracellular guanylyl cyclase domain, which converts GTP to cyclic GMP. This catalytic step is the signal-transmitting component of GO:0016941, because it initiates a change in cell activity after peptide binding. The structural transition that couples hormone recognition to cyclase activation has been characterised for NPR-A, linking the binding event to enzymatic output. NPR-C lacks this cyclase activity and instead modulates peptide availability, which indirectly shapes the activity of NPR-A and NPR-B.
Cyclic GMP effector signalling
In simple terms: The signalling molecule made by the receptor then tells the cell what to do.
Cyclic GMP produced by NPR-A and NPR-B activates downstream effectors such as cyclic GMP-dependent protein kinases, phosphodiesterases and ion channels, which together change contractility, growth and electrophysiology. In the atrium, NPR-B signalling controls cyclic AMP via phosphodiesterase 2, and this crosstalk protects against atrial fibrillation. Augmentation of NPR-A and NPR-B cyclic GMP signalling is being evaluated as a therapeutic strategy in heart failure, which underscores the functional importance of this step.
Clearance and feedback by NPR-C
In simple terms: A third receptor acts like a sponge that removes the hormone and tunes the signal.
NPR-C binds natriuretic peptides and mediates their clearance, thereby limiting the amount of ligand available to activate NPR-A and NPR-B. This clearance function is part of the broader natriuretic peptide axis and provides negative feedback on GO:0016941 by reducing ligand occupancy of the signalling receptors. Because NPR-C also participates in peptide internalisation and degradation, its activity influences the duration and amplitude of receptor-mediated cyclic GMP responses.
Integration with the renin-angiotensin and neprilysin systems
In simple terms: The receptor signal is balanced against other hormone systems that raise or lower blood pressure.
Natriuretic peptide receptor activity is integrated with the renin-angiotensin-aldosterone system and with neprilysin, the enzyme that degrades natriuretic peptides. Angiotensin receptor-neprilysin inhibitors increase natriuretic peptide availability and thereby enhance receptor-mediated signalling, illustrating how the activity is modulated pharmacologically. This integration means that GO:0016941 should be interpreted in the context of competing vasoconstrictor and volume-retaining pathways.
Key Genes Involved in GO:0016941 natriuretic peptide receptor activity
The genes below encode the receptors, ligands and downstream effectors that define or modulate GO:0016941 natriuretic peptide receptor activity.
| Gene | Major Role | Research Relevance |
|---|---|---|
| NPR1 | Encodes NPR-A, a membrane guanylyl cyclase that binds ANP and BNP and produces cyclic GMP | Central receptor for cardiac and renal natriuretic peptide responses; target for heart failure studies |
| NPR2 | Encodes NPR-B, a guanylyl cyclase that binds CNP and produces cyclic GMP | Linked to atrial electrophysiology and cyclic AMP crosstalk via phosphodiesterase 2 |
| NPR3 | Encodes NPR-C, a clearance receptor that binds ANP, BNP and CNP | Modulates ligand availability and duration of receptor signalling |
| NPPA | Encodes atrial natriuretic peptide (ANP), a ligand for NPR-A | Biomarker and ligand for receptor activation studies |
| NPPB | Encodes B-type natriuretic peptide (BNP), a ligand for NPR-A | Clinically used biomarker and ligand for NPR-A signalling |
| NPPC | Encodes C-type natriuretic peptide (CNP), a ligand for NPR-B | Ligand for NPR-B-dependent cyclic GMP signalling |
| MME | Encodes neprilysin, the enzyme that degrades natriuretic peptides | Pharmacological target of angiotensin receptor-neprilysin inhibitors |
| PDE2A | Encodes phosphodiesterase 2, which controls atrial cyclic AMP downstream of NPR-B | Modifier of NPR-B signalling in atrial fibrillation models |
| PRKG1 | Encodes cyclic GMP-dependent protein kinase I, a downstream effector of cyclic GMP | Readout of NPR-A and NPR-B pathway activation |
| PRKG2 | Encodes cyclic GMP-dependent protein kinase II, a downstream effector in multiple tissues | Effector of cyclic GMP signalling initiated by receptor activity |
| GUCY1A1 | Encodes a subunit of soluble guanylate cyclase, a parallel cyclic GMP source | Relevant to interpreting guanylate cyclase stimulator studies |
| GUCY1B1 | Encodes a subunit of soluble guanylate cyclase, a parallel cyclic GMP source | Context for cyclic GMP-targeted therapeutics |
| AGT | Encodes angiotensinogen, a component of the renin-angiotensin system that opposes natriuretic peptide effects | Context for combination therapies targeting the natriuretic peptide axis |
| REN | Encodes renin, the rate-limiting enzyme of the renin-angiotensin system | Counter-regulatory pathway in cardiovascular models |
| ACE | Encodes angiotensin-converting enzyme, which modulates angiotensin II and bradykinin | Comparator pathway in heart failure pharmacology |
| EDN1 | Encodes endothelin-1, a vasoconstrictor that opposes natriuretic peptide vasodilation | Vascular tone context for receptor activity studies |
| NOS3 | Encodes endothelial nitric oxide synthase, which influences cyclic GMP signalling | Crosstalk with cyclic GMP pathways in vascular models |
How Is natriuretic peptide receptor activity Regulated?
GO:0016941 natriuretic peptide receptor activity is regulated at multiple levels. Ligand availability is controlled by secretion of ANP and BNP from cardiomyocytes in response to wall stress and by neprilysin-mediated degradation, which is the pharmacological target of angiotensin receptor-neprilysin inhibitors. Receptor abundance and sensitivity are modulated by NPR-C-mediated clearance, which reduces the pool of peptide available to activate NPR-A and NPR-B. Downstream, cyclic GMP levels are shaped by phosphodiesterases; in the atrium, phosphodiesterase 2 controls cyclic AMP downstream of NPR-B and thereby influences atrial arrhythmogenesis. Pharmacological augmentation of NPR-A and NPR-B cyclic GMP signalling is an active therapeutic strategy in heart failure, indicating that receptor output can be enhanced independently of ligand supply. Soluble guanylate cyclase stimulators such as riociguat act on a parallel cyclic GMP source, which is relevant when interpreting receptor-specific versus global cyclic GMP effects.
natriuretic peptide receptor activity and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| NPR1 | Heart failure and cardiac remodelling | NPR1 knockout and knock-in cardiomyocyte lines with cyclic GMP readout |
| NPR2 | Atrial fibrillation via atrial cyclic AMP control | NPR2 knockout atrial cardiomyocyte models with phosphodiesterase 2 perturbation |
| NPR3 | Natriuretic peptide clearance and cardiovascular homeostasis | NPR3 knockout cells to measure ligand availability and receptor output |
| MME | Heart failure pharmacology via neprilysin inhibition | MME knockout or point-mutation cells treated with receptor ligands |
| GUCY1A1 | Pulmonary arterial hypertension and cyclic GMP signalling | Soluble guanylate cyclase reporter cells for stimulator studies |
Heart failure and cardiac remodelling
Natriuretic peptides are released from the heart in response to wall stress and act through NPR-A to promote natriuresis, vasodilation and anti-fibrotic effects, making GO:0016941 a central node in heart failure biology. Angiotensin receptor-neprilysin inhibitors increase natriuretic peptide availability and enhance receptor-mediated cyclic GMP signalling, and augmentation of NPR-A and NPR-B signalling is being pursued as a therapeutic strategy in heart failure. These observations link the molecular function directly to clinical outcomes and to drug development.
Atrial fibrillation and electrophysiology
NPR-B protects against atrial fibrillation by controlling atrial cyclic AMP via phosphodiesterase 2, demonstrating that natriuretic peptide receptor activity influences cardiac electrical behaviour beyond hemodynamics. This finding expands the disease relevance of GO:0016941 from pump function to arrhythmia mechanisms and suggests that receptor-selective modulation could have antiarrhythmic effects.
Pulmonary arterial hypertension and vascular disease
Cyclic GMP signalling is a validated therapeutic axis in pulmonary arterial hypertension, as shown by the efficacy of the soluble guanylate cyclase stimulator riociguat. Because NPR-A and NPR-B also raise cyclic GMP, natriuretic peptide receptor activity is mechanistically adjacent to this pathway and is relevant to vascular remodelling and tone. Engineered receptor-selective peptides such as CRRL269 further illustrate how targeting this activity can be refined for vascular indications.
Biomarker and diagnostic context
ANP and BNP are established cardiac biomarkers, and their measurement reflects the activation of the natriuretic peptide system that includes GO:0016941. Understanding receptor activity helps interpret biomarker levels, because receptor occupancy, clearance by NPR-C and degradation by neprilysin all influence the relationship between peptide concentration and biological effect.
From natriuretic peptide receptor activity-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does loss of NPR1 abolish natriuretic peptide-induced cyclic GMP? | NPR1 knockout cell line with cGMP assay |
| Which ectodomain residues determine ligand selectivity? | NPR1 point-mutation knock-in lines guided by structural data |
| Can a receptor-selective peptide activate NPR-A without NPR-B? | Knock-in reporter cells expressing tagged NPR-A and NPR-B |
| Does NPR-B control atrial cyclic AMP via phosphodiesterase 2? | NPR2 knockout atrial cardiomyocyte model with PDE2A perturbation |
| Does NPR-C clearance limit receptor signalling? | NPR3 overexpression and knockout isogenic lines |
| Can cyclic GMP signalling be enhanced pharmacologically? | Reporter cells treated with guanylate cyclase stimulators and receptor ligands |
How to Study the natriuretic peptide receptor activity Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Radioligand binding assay | Peptide-receptor interaction affinity and selectivity | Comparing NPR-A, NPR-B and NPR-C ligand preferences |
| Cyclic GMP immunoassay | Intracellular cyclic GMP concentration after receptor activation | Functional readout of NPR-A and NPR-B activity |
| Genetically encoded cGMP reporter | Real-time cyclic GMP dynamics in living cells | Time-course analysis of receptor stimulation |
| CRISPR knockout | Loss-of-function phenotype for NPR1, NPR2 or NPR3 | Testing causality of receptor activity in disease models |
| CRISPR point mutation | Effect of specific receptor residues on ligand recognition | Mapping ectodomain determinants of hormone selectivity |
| Knock-in reporter tagging | Receptor localisation and expression level | Tracking endogenous NPR-A or NPR-B in cells |
| Phosphoproteomics | Downstream phosphorylation changes after cyclic GMP elevation | Mapping effector networks of receptor signalling |
| Phenotypic atrial cardiomyocyte assay | Electrical and cyclic AMP responses to NPR-B signalling | Atrial fibrillation mechanism studies |
Receptor binding and ligand interaction assays
Radioligand or fluorescent peptide binding assays measure the first step of GO:0016941, namely combination of a natriuretic peptide with its receptor. Such assays can compare NPR-A, NPR-B and NPR-C selectivity and can be combined with structural analysis of hormone recognition. They are typically performed in membrane preparations or intact cells expressing the receptor of interest.
Cyclic GMP quantification
Because NPR-A and NPR-B are guanylyl cyclases, cyclic GMP measurement is the most direct functional readout of receptor activity. Enzyme immunoassays, mass spectrometry or genetically encoded cyclic GMP reporters can be used to quantify receptor output after ligand stimulation, and these readouts are central to studies of heart failure therapeutics.
Genetic perturbation with CRISPR
CRISPR knockout, point mutation, knock-in and overexpression allow causal testing of NPR1, NPR2 and NPR3 in isogenic backgrounds. For example, NPR2 knockout has been used to probe atrial cyclic AMP control and arrhythmia protection, while NPR-A and NPR-B augmentation studies inform heart failure strategies. These models are essential for distinguishing receptor-specific effects from parallel cyclic GMP sources.
Phosphoproteomics and downstream effector mapping
Cyclic GMP produced by receptor activity activates protein kinases and phosphodiesterases, so phosphoproteomics and targeted assays can map the downstream network. Combining these methods with receptor perturbation clarifies which cellular changes are directly attributable to GO:0016941 rather than to crosstalk with other pathways.
How CRISPR Can Be Used to Study GO:0016941 natriuretic peptide receptor activity
Knockout
CRISPR knockout of NPR1, NPR2 or NPR3 removes the receptor and provides a clean loss-of-function test of GO:0016941. Such models are used to determine whether a cellular response to natriuretic peptide depends on a specific receptor, and they complement pharmacological tools that act on the same pathway. Knockout of NPR2 in atrial models has been used to show that NPR-B signalling controls atrial cyclic AMP and protects against atrial fibrillation.
Point Mutation
Point-mutation knock-in allows precise testing of receptor residues implicated in hormone recognition and catalytic activation. Structural insights into NPR-A hormone recognition provide a template for selecting residues that determine ligand selectivity or cyclase coupling, and CRISPR point mutation can validate these predictions in cells. This approach is valuable when a complete knockout would eliminate both binding and signalling functions.
Knock-in
Knock-in of tagged or reporter-linked receptors enables tracking of endogenous NPR-A, NPR-B or NPR-C expression, localisation and turnover. Tagged knock-in lines can be combined with cyclic GMP readouts to correlate receptor abundance with signalling output, which is useful for interpreting how NPR-C clearance shapes the activity of the signalling receptors.
Overexpression
Overexpression of NPR1, NPR2 or NPR3 increases receptor availability and can amplify or dampen natriuretic peptide responses depending on the receptor. Overexpression models are used to test whether enhanced receptor signalling is sufficient to change disease-relevant phenotypes, and they complement therapeutic strategies that aim to augment NPR-A and NPR-B cyclic GMP signalling in heart failure. They are also useful for testing receptor-selective peptides such as CRRL269.
How EDITGENE Supports natriuretic peptide receptor activity Research
Researchers studying natriuretic peptide receptor activity-related genes often need to determine whether a candidate gene is causally involved in ligand recognition, cyclic GMP production or downstream cellular responses. EDITGENE provides CRISPR-based cell model services that allow this question to be answered in isogenic, disease-relevant backgrounds, with readouts that map directly onto GO:0016941.
Contact EDITGENE today to design your custom CRISPR model for natriuretic peptide receptor activity research.
Frequently Asked Questions About natriuretic peptide receptor activity
What is GO:0016941 natriuretic peptide receptor activity?
GO:0016941 is a Gene Ontology molecular function defined as combining with a natriuretic peptide and transmitting the signal to initiate a change in cell activity. It is executed by receptors such as NPR-A and NPR-B, which produce cyclic GMP after ligand binding.
What genes are involved in natriuretic peptide receptor activity?
The core genes are NPR1 (NPR-A), NPR2 (NPR-B) and NPR3 (NPR-C), with ligands encoded by NPPA, NPPB and NPPC, and modifying enzymes such as MME and PDE2A.
Which receptors have natriuretic peptide receptor activity?
NPR-A and NPR-B are guanylyl cyclases that produce cyclic GMP upon peptide binding, while NPR-C binds natriuretic peptides primarily for clearance.
What second messenger is produced by natriuretic peptide receptor activity?
Cyclic GMP is produced by the guanylyl cyclase domain of NPR-A and NPR-B after ligand binding.
How is natriuretic peptide receptor activity studied experimentally?
Common approaches include radioligand binding assays, cyclic GMP quantification, CRISPR knockout or knock-in of NPR1, NPR2 and NPR3, and phosphoproteomic mapping of downstream effectors.
Why is natriuretic peptide receptor activity important in heart failure?
Natriuretic peptides promote natriuresis and vasodilation through NPR-A, and therapies that increase peptide availability or augment NPR-A and NPR-B cyclic GMP signalling are used or investigated in heart failure.
Does NPR-B signalling affect atrial fibrillation?
Yes, NPR-B protects against atrial fibrillation by controlling atrial cyclic AMP via phosphodiesterase 2.
What is the role of NPR-C in this pathway?
NPR-C acts as a clearance receptor that binds natriuretic peptides and limits their availability to activate NPR-A and NPR-B.
Can CRISPR be used to study natriuretic peptide receptor activity?
Yes, CRISPR knockout, point mutation, knock-in and overexpression of NPR1, NPR2 and NPR3 allow causal testing of receptor function and downstream cyclic GMP responses.
What drugs target the natriuretic peptide receptor pathway?
Angiotensin receptor-neprilysin inhibitors increase natriuretic peptide availability, and soluble guanylate cyclase stimulators such as riociguat act on the cyclic GMP pathway downstream of receptor activation.
Conclusion
GO:0016941 natriuretic peptide receptor activity captures the molecular event in which natriuretic peptides bind their receptors and trigger intracellular signalling, principally through cyclic GMP produced by NPR-A and NPR-B. This activity is central to cardiovascular homeostasis and is directly implicated in heart failure, atrial fibrillation and pulmonary arterial hypertension, where both ligand availability and receptor output are therapeutic targets. Because the pathway is genetically tractable and enzymatically measurable, CRISPR-engineered cell models provide a rigorous route to dissect receptor-specific mechanisms and to prioritise new interventions.
References
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- 3. Potter LR et al.. 2009. Natriuretic peptides: their structures, receptors, physiologic functions and therapeutic applications.. Handb Exp Pharmacol PMID: 19089336
- 4. Dorey TW et al.. 2023. Natriuretic Peptide Receptor B Protects Against Atrial Fibrillation by Controlling Atrial cAMP Via Phosphodiesterase 2.. Circ Arrhythm Electrophysiol 16(11):e012199 PMID: 37933567
- 5. Ogawa H et al.. 2024. Structural insight into hormone recognition by the natriuretic peptide receptor-A.. FEBS J 291(10):2273-2286 PMID: 38437249
- 6. Ghofrani HA et al.. 2013. Riociguat for the treatment of pulmonary arterial hypertension.. N Engl J Med 369(4):330-40 PMID: 23883378
- 7. Chen Y et al.. 2019. CRRL269.. Circ Res 124(10):1462-1472 PMID: 30929579
- 8. Ajay A et al.. 2023. Augmentation of natriuretic peptide (NP) receptor A and B (NPR-A and NPR-B) and cyclic guanosine monophosphate (cGMP) signalling as a therapeutic strategy in heart failure.. Expert Opin Investig Drugs 32(12):1157-1170 PMID: 38032188
