ArticleCellular and molecular neurobiology2010
Catestatin improves post-ischemic left ventricular function and decreases ischemia/reperfusion injury in heart.
Article in Cellular and molecular neurobiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 72 citations in OpenAlex.
- Catestatin-A Novel Predictor of Left Ventricular Remodeling After Acute Myocardial Infarction.Scientific reports · 2017Trial
- Catestatin restores cardiac metabolic flexibility and enhances mitochondrial function.Communications biology · 2026Article
- Catestatin in Cardiovascular Diseases.International journal of molecular sciences · 2025Review
- Mitochondrial-derived peptides: Antidiabetic functions and evolutionary perspectives.Peptides · 2024Review
- Chromogranin A and its derived peptides: potential regulators of cholesterol homeostasis.Cellular and molecular life sciences : CMLS · 2023Review
- 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
- Review
- The Emerging Roles of Chromogranins and Derived Polypeptides in Atherosclerosis, Diabetes, and Coronary Heart Disease.International journal of molecular sciences · 2021Review
- Immunosuppression of Macrophages Underlies the Cardioprotective Effects of CST (Catestatin).Hypertension (Dallas, Tex. : 1979) · 2021Article
- Neurohumoral, cardiac and inflammatory markers in the evaluation of heart failure severity and progression.Journal of geriatric cardiology : JGC · 2021Article
- Chromogranin A and its fragments in cardiovascular, immunometabolic, and cancer regulation.Annals of the New York Academy of Sciences · 2019Review
- Single-territory incomplete surgical revascularization improves regional wall motion of remote ventricular areas: results from a propensity-matched study.Journal of geriatric cardiology : JGC · 2018Article
- Circulating chromogranin A and its fragments as diagnostic and prognostic disease markers.Pflugers Archiv : European journal of physiology · 2018Review
- Chromogranins: from discovery to current times.Pflugers Archiv : European journal of physiology · 2018Review
- Catestatin as a Target for Treatment of Inflammatory Diseases.Frontiers in immunology · 2018Review
- 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
- Chromogranin A Regulation of Obesity and Peripheral Insulin Sensitivity.Frontiers in endocrinology · 2017Review
- Nesfatin-1: a new energy-regulating peptide with pleiotropic functions. Implications at cardiovascular level.Endocrine · 2016Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Chromogranin A (CgA)-derived anti-hypertensive peptide catestatin (CST) antagonizes catecholamine secretion, and is a negative myocardial inotrope acting via a nitric oxide-dependent mechanism. It is not known whether CST contributes to ischemia/reperfusion injury or is a component of a cardioprotective response to limit injury. Here, we tested whether CST by virtue of its negative inotropic activity improves post-ischemic cardiac function and cardiomyocyte survival. Three groups of isolated perfused hearts from adult Wistar rats underwent 30-min ischemia and 120-min reperfusion (I/R, Group 1), or were post-conditioned by brief ischemic episodes (PostC, 5-cycles of 10-s I/R at the beginning of 120-min reperfusion, Group 2), or with exogenous CST (75 nM for 20 min, CST-Post, Group-3) at the onset of reperfusion. Perfusion pressure and left ventricular pressure (LVP) were monitored. Infarct size was evaluated with nitroblue-tetrazolium staining. The CST (5 nM) effects were also tested in simulated ischemia/reperfusion experiments on cardiomyocytes isolated from young-adult rats, evaluating cell survival with propidium iodide labeling. Infarct size was 61 ± 6% of risk area in hearts subjected to I/R only. PostC reduced infarct size to 34 ± 5%. Infarct size in CST-Post was 36 ± 3% of risk area (P < 0.05 respect to I/R). CST-Post reduced post-ischemic rise of diastolic LVP, an index of contracture, and significantly improved post-ischemic recovery of developed LVP. In isolated cardiomyocytes, CST increased the cell viability rate by about 65% after simulated ischemia/reperfusion. These results suggest a novel cardioprotective role for CST, which appears mainly due to a direct reduction of post-ischemic myocardial damages and dysfunction, rather than to an involvement of adrenergic terminals and/or endothelium.
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Registered trials
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