ArticlePloS one2015
Catestatin exerts direct protective effects on rat cardiomyocytes undergoing ischemia/reperfusion by stimulating PI3K-Akt-GSK3β pathway and preserving mitochondrial membrane potential.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
- Catestatin-A Novel Predictor of Left Ventricular Remodeling After Acute Myocardial Infarction.Scientific reports · 2017Trial
- Modified mRNA-Based Therapeutic Strategies for Myocardial Ischemia-Reperfusion Injury.International journal of molecular sciences · 2025Review
- Small Extracellular Vesicles from Breast Cancer Cells Induce Cardiotoxicity.International journal of molecular sciences · 2025Article
- The physiological anti-hypertensive peptide catestatin and its common human variant Gly364Ser: differential cardiovascular effects in a rat model of hypertension.Bioscience reports · 2024Article
- Outcomes of hypothalamic oxytocin neuron-driven cardioprotection after acute myocardial infarction.Basic research in cardiology · 2023Article
- Chromogranin A and its derived peptides: potential regulators of cholesterol homeostasis.Cellular and molecular life sciences : CMLS · 2023Review
- Prognostic differences of catestatin among young and elderly patients with acute myocardial infarction.World journal of emergency medicine · 2022Article
- Review
- Article
- Sympathetic nervous system activation and heart failure: Current state of evidence and the pathophysiology in the light of novel biomarkers.World journal of cardiology · 2020Review
- Catestatin reverses the hypertrophic effects of norepinephrine in H9c2 cardiac myoblasts by modulating the adrenergic signaling.Molecular and cellular biochemistry · 2020Article
- Chromogranin A and its fragments in cardiovascular, immunometabolic, and cancer regulation.Annals of the New York Academy of Sciences · 2019Review
- Catestatin Induces Glucose Uptake and GLUT4 Trafficking in Adult Rat Cardiomyocytes.BioMed research international · 2018Article
- Glycosylated Chromogranin A: Potential Role in the Pathogenesis of Heart Failure.Current heart failure reports · 2017Review
- The role of neuropeptides in adverse myocardial remodeling and heart failure.Cellular and molecular life sciences : CMLS · 2017Review
- CSPGs inhibit axon branching by impairing mitochondria-dependent regulation of actin dynamics and axonal translation.Developmental neurobiology · 2017Article
- Chromogranin A Regulation of Obesity and Peripheral Insulin Sensitivity.Frontiers in endocrinology · 2017Review
- Roles of Endoplasmic Reticulum Stress in NECA-Induced Cardioprotection against Ischemia/Reperfusion Injury.Oxidative medicine and cellular longevity · 2017Article
- Identification of novel loci affecting circulating chromogranins and related peptides.Human molecular genetics · 2017Article
- Ilexsaponin A attenuates ischemia-reperfusion-induced myocardial injury through anti-apoptotic pathway.PloS one · 2017Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Catestatin (Cst) is a 21-amino acid peptide deriving from Chromogranin A. Cst exerts an overall protective effect against an excessive sympathetic stimulation of cardiovascular system, being able to antagonize catecholamine secretion and to reduce their positive inotropic effect, by stimulating the release of nitric oxide (NO) from endothelial cells. Moreover, Cst reduces ischemia/reperfusion (I/R) injury, improving post-ischemic cardiac function and cardiomyocyte survival. To define the cardioprotective signaling pathways activated by Cst (5 nM) we used isolated adult rat cardiomyocytes undergoing simulated I/R. We evaluated cell viability rate with propidium iodide labeling and mitochondrial membrane potential (MMP) with the fluorescent probe JC-1. The involvement of Akt, GSK3β, eNOS and phospholamban (PLN) cascade was studied by immunofluorescence. The role of PI3K-Akt/NO/cGMP pathway was also investigated by using the pharmacological blockers wortmannin (Wm), L-NMMA and ODQ. Our experiments revealed that Cst increased cell viability rate by 65% and reduced cell contracture in I/R cardiomyocytes. Wm, L-NMMA and ODQ limited the protective effect of Cst. The protective outcome of Cst was related to its ability to maintain MMP and to increase AktSer473, GSK3βSer9, PLNThr17 and eNOSSer1179 phosphorylation, while treatment with Wm abolished these effects. Thus, the present results show that Cst is able to exert a direct action on cardiomyocytes and give new insights into the molecular mechanisms involved in its protective effect, highlighting the PI3K/NO/cGMP pathway as the trigger and the MMP preservation as the end point of its action.
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