CNP Preserves Cardiac and Vascular Function in Sepsis - A Promising Therapeutic Target

CNP mainly operates through autocrine and paracrine mechanisms and is crucial for promoting bone growth (1). Recent studies have deepened our understanding of CNP’s role in cardiovascular regulation (2). It exhibits antifibrotic effects across various organs (3), induces vasodilation in microcirculations, improves myocardial relaxation, and has anti-inflammatory properties (4). These benefits have shown therapeutic potential in experimental models of pulmonary hypertension, myocardial infarction, and organ fibrosis (4).

CNP Preserves Cardiac and Vascular Function in Sepsis – A Promising Therapeutic Target

About NT-proCNP

NT-proCNP is generated through the cleavage of a 103-amino acid prohormone called proCNP, resulting in the production of the amino-terminal fragment (NT-proCNP) and the biologically active CNP peptides (5) . NTproCNP has a longer half-life and is present in the blood at higher concentrations than biologically active CNP (6, 7). 

CNP Preserves Cardiac and Vascular Function in Sepsis – A Promising Therapeutic Target

Our NT-proCNP ELISA was a key tool in a recent study (8) examining the potential of C-Type Natriuretic Peptide (CNP) in sepsis treatment. The study demonstrates that CNP helps preserve both vascular and cardiac function during sepsis, offering promising insights into improving patient outcomes.

C-Type Natriuretic Peptide Preserves Vascular and Cardiac Function in Sepsis, Moyes AJ et al., Hypertension, 2026.

Key findings:

• Genetic deletion of #CNP worsens disease severity in experimental sepsis.
• CNP levels increase in sepsis and correlate with lung hypoxemia.
• Therapeutic administration of CNP significantly reduces sepsis progression.

Abstract

Background: Sepsis is a life-threatening condition and a major cause of mortality in intensive care units worldwide, a clear unmet medical need. CNP (C-type natriuretic peptide) regulates inflammation and cardiovascular homeostasis, but its involvement in sepsis pathogenesis is not fully elucidated. This study investigated the intrinsic role of CNP, and therapeutic potential of the peptide, in offsetting the pathogenesis of sepsis.

Methods: Plasma concentrations of CNP, and its N-terminal cleavage product NT-proCNP (N-terminal pro-CNP), were measured in sepsis patients. Cardiac function, vascular hemodynamics, endothelial integrity, and biomarkers of inflammation were analyzed in wild-type, endothelium-restricted (ecCNP^-/-), or cardiomyocyte-restricted (cmCNP^-/-) CNP knockout animals, or global NPR (natriuretic peptide receptor)-C^-/- deficient mice, in etiologically distinct models of sepsis. CNP (0.2 mg/kg per d) was infused to rescue any adverse phenotype and probe therapeutic potential.

Results: Circulating [NT-proCNP] increased in sepsis patients and was associated with reduced disease severity. ecCNP^-/- mice exhibited an aggravated phenotype compared with wild-type mice in experimental sepsis, exemplified by impaired microcirculatory flow, edema, and increased expression of inflammatory biomarkers. In addition, cmCNP^-/- animals showed overt cardiac dysfunction following lipopolysaccharide treatment. This worsened phenotype was mirrored in NPR-C^-/- mice, implying that this cognate NPR subtype underpins the salutary actions of endogenous CNP. Pharmacological CNP administration improved microvascular perfusion, cardiac output, and inflammation in wild-type and ecCNP^-/-, but not NPR-C^-/-, mice.

Conclusions: Endogenous CNP plays a protective role in sepsis by preserving microvascular perfusion, reducing inflammation, maintaining endothelial integrity, and sustaining cardiac function via NPR-C. Pharmacologically targeting CNP signaling warrants further evaluation as a potential therapeutic opportunity in sepsis.

NT-proCNP #ELISA kit  (cat.no. BI-20812)

TRUSTED – widely cited

RELIABLE – full validation package

FLEXIBEL – for serum and plasma samples, protocols available for urine, cell culture and non-human samples

Literature

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2. C-type natriuretic peptide (CNP): The cardiovascular system and beyond. Dickinson YA, Moyes AJ, Hobbs AJ.Pharmacol Ther. 2024 Oct;262:108708. doi: 10.1016/j.pharmthera.2024.108708. Epub 2024 Aug 21. PMID: 39154787.
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8. C-Type Natriuretic Peptide Preserves Vascular and Cardiac Function in Sepsis. Moyes AJ, Sand C, Young L, Pérez-Ternero C, Salam AT, Baliga RS, Mohammad S, Antcliffe DB, Gordon AC, Aubdool AA, Hobbs AJ.Hypertension. 2026 Jun;83(6):e25938. doi: 10.1161/HYPERTENSIONAHA.125.25938. Epub 2026 Feb 4. PMID: 41636071; PMCID: PMC13189390.