ArticleAmerican journal of physiology. Heart and circulatory physiology2008
Catestatin (chromogranin A344-364) is a novel cardiosuppressive agent: inhibition of isoproterenol and endothelin signaling in the frog heart.
Article in American journal of physiology. Heart and circulatory physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
26 citing papers in PubMed, 72 citations in OpenAlex.
- Catestatin-A Novel Predictor of Left Ventricular Remodeling After Acute Myocardial Infarction.Scientific reports · 2017Trial
- Direct vasoactive effects of the chromogranin A (CHGA) peptide catestatin in humans in vivo.Clinical and experimental hypertension (New York, N.Y. : 1993) · 2010Trial
- Catestatin restores cardiac metabolic flexibility and enhances mitochondrial function.Communications biology · 2026Article
- A Tri-Culture Heart-on-a-Chip Platform With iPSC-Derived Cardiac Cells for Predictive Cardiotoxicity Testing.Advanced healthcare materials · 2026Article
- Chromogranin A and its derived peptides: potential regulators of cholesterol homeostasis.Cellular and molecular life sciences : CMLS · 2023Review
- Catestatin Protects Against Diastolic Dysfunction by Attenuating Mitochondrial Reactive Oxygen Species Generation.Journal of the American Heart Association · 2023Article
- Serum Catestatin Concentrations Are Increased in Patients with Atrial Fibrillation.Journal of cardiovascular development and disease · 2023Article
- Prognostic Value of Catestatin in Severe COVID-19: An ICU-Based Study.Journal of clinical medicine · 2022Article
- Review
- Plasma catestatin level predicts sPESI score and mortality in acute pulmonary embolism.Archives of medical sciences. Atherosclerotic diseases · 2020Article
- Chromogranin A and its fragments in cardiovascular, immunometabolic, and cancer regulation.Annals of the New York Academy of Sciences · 2019Review
- Catestatin in Acutely Decompensated Heart Failure Patients: Insights from the CATSTAT-HF Study.Journal of clinical medicine · 2019Article
- Glycosylated Chromogranin A: Potential Role in the Pathogenesis of Heart Failure.Current heart failure reports · 2017Review
- Catestatin Gly364Ser Variant Alters Systemic Blood Pressure and the Risk for Hypertension in Human Populations via Endothelial Nitric Oxide Pathway.Hypertension (Dallas, Tex. : 1979) · 2016Article
- Catestatin attenuates endoplasmic reticulum induced cell apoptosis by activation type 2 muscarinic acetylcholine receptor in cardiac ischemia/reperfusion.Scientific reports · 2015Article
- Microfluidic heart on a chip for higher throughput pharmacological studies.Lab on a chip · 2013Article
- Toad heart utilizes exclusively slow skeletal muscle troponin T: an evolutionary adaptation with potential functional benefits.The Journal of biological chemistry · 2012Article
- Catestatin (chromogranin A(352-372)) and novel effects on mobilization of fat from adipose tissue through regulation of adrenergic and leptin signaling.The Journal of biological chemistry · 2012Article
- The extended granin family: structure, function, and biomedical implications.Endocrine reviews · 2011Review
- Chromogranin/secretogranin proteins in murine heart: myocardial production of chromogranin A fragment catestatin (Chga(364-384)).Cell and tissue research · 2010Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The catecholamine release-inhibitory catestatin [Cts; human chromogranin (Cg) A(352-372), bovine CgA(344-364)] is a vasoreactive and anti-hypertensive peptide derived from CgA. Using the isolated avascular frog heart as a bioassay, in which the interactions between the endocardial endothelium and the subjacent myocardium can be studied without the confounding effects of the vascular endothelium, we tested the direct cardiotropic effects of bovine Cts and its interaction with beta-adrenergic (isoproterenol, ISO) and endothelin-1 (ET-1) signaling. Cts dose-dependently decreased stroke volume and stroke work, with a threshold concentration of 11 nM, approaching the in vivo level of the peptide. Cts reduced contractility by inhibiting phosphorylation of phospholamban (PLN). Furthermore, the Cts effect was abolished by pretreatment with either nitric oxide synthase (N(G)-monomethyl-l-arginine) or guanylate cyclase (ODQ) inhibitors, or an ET(B) receptor (ET(BR)) antagonist (BQ-788). Cts also noncompetitively inhibited the positive inotropic action of ISO. In addition, Cts inhibited the positive inotropic effect of ET-1, mediated by ET(A) receptors, and did not alter the negative inotropic ET-1 influence mediated by ET(BR). Cts action through ET(BR) was further suggested when, in the presence of BQ-788, Cts failed to inhibit the positive inotropism of both ISO and ET-1 stimulation and PLN phosphorylation. We concluded that the cardiotropic actions of Cts, including the beta-adrenergic and ET-1 antagonistic effects, support a novel role of this peptide as an autocrine-paracrine modulator of cardiac function, particularly when the stressed heart becomes a preferential target of both adrenergic and ET-1 stimuli.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.