The cardiac natriuretic peptides (NPs) control pivotal physiological actions such as fluid and electrolyte balance, cardiovascular homeostasis, and adipose tissue metabolism by activating their receptor enzymes [natriuretic peptide receptor-A (NPRA) and natriuretic peptide receptor-B (NPRB)]. These receptors are homodimers that generate intracellular cyclic guanosine monophosphate (cGMP). The natriuretic peptide receptor-C (NPRC), nicknamed the clearance receptor, lacks a guanylyl cyclase domain; instead, it can bind the NPs to internalize and degrade them. The conventional paradigm is that by competing for and internalizing NPs, NPRC blunts the ability of NPs to signal through NPRA and NPRB. Here we show another previously unknown mechanism by which NPRC can interfere with the cGMP signaling function of the NP receptors. By forming a heterodimer with monomeric NPRA or NPRB, NPRC can prevent the formation of a functional guanylyl cyclase domain and thereby suppress cGMP production in a cell-autonomous manner.
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http://dx.doi.org/10.1073/pnas.2307882120 | DOI Listing |
Cardiovasc Diabetol
January 2025
Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Background: Diabetic myocardial disorder (DbMD, evidenced by abnormal echocardiography or cardiac biomarkers) is a form of stage B heart failure (SBHF) at high risk for progression to overt HF. SBHF is defined by abnormal LV morphology and function and/or abnormal cardiac biomarker concentrations.
Objective: To compare the evolution of four DbMD groups based on biomarkers alone, systolic and diastolic dysfunction alone, or their combination.
Pharm Res
January 2025
Beijing Hospital, National Center of Gerontology, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Purpose: Recombinant human B-type natriuretic peptide (rhBNP) has been extensively proven to be an effective mean of heart failure (HF) therapy, but its clinical application is limited by its very short half-life. This study aims to combine in vitro transcribed mRNA (IVT mRNA) and fusion protein technology to develop a rhBNP-Fc mRNA drug with long half-life, high efficiency and few side effects to treat HF.
Methods: The rhBNP-Fc fusion mRNA with IgG4-Fc sequence was produced by IVT technology.
JACC Asia
December 2024
Division of Cardiology, Department of Internal Medicine, Chang Gung Memorial Hospital at Linkou, and Chang Gung University College of Medicine, Taoyuan, Taiwan.
Background: Few studies have incorporated echocardiography and laboratory data to predict clinical outcomes in heart failure with preserved ejection fraction (HFpEF).
Objectives: This study aimed to use machine learning to find predictors of heart failure (HF) hospitalization and cardiovascular (CV) death in HFpEF.
Methods: From the Chang Gung Research Database in Taiwan, 6,092 HFpEF patients (2,898 derivation, 3,194 validation) identified between 2008 and 2017 were followed until 2019.
Toxicol Rep
June 2025
University of Dschang, Department of Animal Biology, Dschang, Dschang, Cameroon.
The seeds of are popularly used in the management of cardiovascular conditions. This study was undertaken to evaluate the capacity of the seed ethanolic extract of (EE) to prevent the development of cardiac hypertrophy in rats. Isoproterenol (0.
View Article and Find Full Text PDFOpen Heart
January 2025
Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.
Background: The role of cyclic guanosine 3',5'-monophosphate (cGMP) after acute myocardial infarction (AMI) is not well understood despite its significance as a second messenger of natriuretic peptides (NPs) in cardiovascular disease. We investigated the association between the NP-cGMP cascade and left ventricular reverse remodelling (LVRR) in anterior AMI.
Methods: 67 patients with their first anterior AMI (median age, 64 years; male, 76%) underwent prospective evaluation of plasma concentrations of the molecular forms of A-type and B-type natriuretic peptide (BNP) and cGMP from immediately after primary percutaneous coronary intervention (PPCI) to 10 months post-AMI.
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