ArticleEndocrinology2008
The antihypertensive chromogranin a peptide catestatin acts as a novel endocrine/paracrine modulator of cardiac inotropism and lusitropism.
Article in Endocrinology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
70 citing papers in PubMed, 146 citations in OpenAlex.
- Functional genetic variants of the catecholamine-release-inhibitory peptide catestatin in an Indian population: allele-specific effects on metabolic traits.The Journal of biological chemistry · 2012Trial
- 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
- The role of chromogranin A cleavage products in onset of type 1 and 2 diabetes.Frontiers in clinical diabetes and healthcare · 2026Review
- Chromogranin A deficiency attenuates tauopathy by altering epinephrine-alpha-adrenergic receptor signaling in PS19 mice.Nature communications · 2025Article
- Catestatin in Cardiovascular Diseases.International journal of molecular sciences · 2025Review
- The physiological anti-hypertensive peptide catestatin and its common human variant Gly364Ser: differential cardiovascular effects in a rat model of hypertension.Bioscience reports · 2024Article
- The Role of Catestatin in Preeclampsia.International journal of molecular sciences · 2024Review
- Mitochondrial-derived peptides: Antidiabetic functions and evolutionary perspectives.Peptides · 2024Review
- 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
- Serum Catestatin Level as a Stratification Assessment Tool in Non-Critical COVID-19 Patients.International journal of environmental research and public health · 2023Article
- Low catestatin as a risk factor for cardiovascular disease - assessment in patients with adrenal incidentalomas.Frontiers in endocrinology · 2023Article
- Review
- Neuropilin-1 and Integrins as Receptors for Chromogranin A-Derived Peptides.Pharmaceutics · 2022Review
- Serum catestatin levels in patients with rheumatoid arthritis.Scientific reports · 2022Observational
- Role of Catestatin in the Cardiovascular System and Metabolic Disorders.Frontiers in cardiovascular medicine · 2022Review
- Gut microbial DNA and immune checkpoint gene Vsig4/CRIg are key antagonistic players in healthy aging and age-associated development of hypertension and diabetes.Frontiers in endocrinology · 2022Article
- Biomarkers of Volume Overload and Edema in Heart Failure With Reduced Ejection Fraction.Frontiers in cardiovascular medicine · 2022Review
- Review
10 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Circulating levels of catestatin (Cts; human chromogranin A352-372) decrease in the plasma of patients with essential hypertension. Genetic ablation of the chromogranin A (Chga) gene in mice increases blood pressure and pretreatment of Chga-null mice with Cts prevents blood pressure elevation, indicating a direct role of Cts in preventing hypertension. This notable vasoreactivity prompted us to test the direct cardiovascular effects and mechanisms of action of wild-type (WT) Cts and naturally occurring human variants (G364S-Cts and P370L-Cts) on myocardial and coronary functions. The direct cardiovascular actions of WT-Cts and human variants were determined using the Langendorff-perfused rat heart. WT-Cts dose-dependently increased heart rate and coronary pressure and decreased left ventricular pressure, rate pressure product and both positive and negative LVdP/dt. WT-Cts not only inhibited phospholamban phosphorylation, but also the inotropic and lusitropic effects of WT-Cts were abolished by chemical inhibition of beta2-adrenergic receptors, Gi/o protein, nitric oxide or cGMP, indicating involvement of beta2-adrenergic receptors-Gi/o protein-nitric oxide-cGMP signaling mechanisms. In contrast, G364S-Cts did not affect basal cardiac performance but abolished isoproterenol-induced positive inotropism and lusitropism. P370L-Cts decreased rate pressure product and inhibited only isoproterenol-induced positive inotropism and lusitropism by 70%. Cts also inhibited endothelin-1-induced positive inotropism and coronary constriction. Taken together, the cardioinhibitory influence exerted on basal mechanical performance and the counterregulatory action against beta-adrenergic and endothelin-1 stimulations point to Cts as a novel cardiac modulator, able to protect the heart against excessive sympathochromaffin overactivation, e.g. hypertensive cardiomyopathy.
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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.