ArticlePloS one2014
Catestatin increases the expression of anti-apoptotic and pro-angiogenetic factors in the post-ischemic hypertrophied heart of SHR.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 15 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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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
15 citing papers in PubMed, 35 citations in OpenAlex.
- Catestatin-A Novel Predictor of Left Ventricular Remodeling After Acute Myocardial Infarction.Scientific reports · 2017Trial
- Mitochondrial-derived peptides: Antidiabetic functions and evolutionary perspectives.Peptides · 2024Review
- Role of Catestatin in the Cardiovascular System and Metabolic Disorders.Frontiers in cardiovascular medicine · 2022Review
- Increased Endogenous Activity of the Renin-Angiotensin System Reduces Infarct Size in the Rats with Early Angiotensin II-dependent Hypertension which Survive the Acute Ischemia/Reperfusion Injury.Frontiers in pharmacology · 2021Article
- Article
- 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
- β-Adrenergic signaling, monoamine oxidase A and antioxidant defence in the myocardium of SHR and SHR-mtBN conplastic rat strains: the effect of chronic hypoxia.The journal of physiological sciences : JPS · 2018Article
- 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
- Emulsified isoflurane postconditioning improves survival and neurological outcomes in a rat model of cardiac arrest.Experimental and therapeutic medicine · 2017Article
- The role of neuropeptides in adverse myocardial remodeling and heart failure.Cellular and molecular life sciences : CMLS · 2017Review
- Chromogranin A Regulation of Obesity and Peripheral Insulin Sensitivity.Frontiers in endocrinology · 2017Review
- Catestatin attenuates endoplasmic reticulum induced cell apoptosis by activation type 2 muscarinic acetylcholine receptor in cardiac ischemia/reperfusion.Scientific reports · 2015Article
- Correlation of plasma catestatin level and the prognosis of patients with acute myocardial infarction.PloS one · 2015Article
- The surging role of Chromogranin A in cardiovascular homeostasis.Frontiers in chemistry · 2014Review
Corrections and comments
- Retraction · 2021-02-04Concerns/Issues about Data · Duplication of/in Image · Error in Image · · see also: https://pubpeer.com/publications/1EA6CF6801C055BCA25132F117413E
- Retracted
Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIn the presence of comorbidities the effectiveness of many cardioprotective strategies is blunted. The goal of this study was to assess in a hypertensive rat model if the early reperfusion with anti-hypertensive and pro-angiogenic Chromogranin A-derived peptide, Catestatin (CST:hCgA352-372; CST-Post), protects the heart via Reperfusion-Injury-Salvage-Kinases (RISK)-pathway activation, limiting infarct-size and apoptosis, and promoting angiogenetic factors (e.g., hypoxia inducible factor, HIF-1α, and endothelial nitric oxide synthase, eNOS, expression). METHODS AND
resultsThe effects of CST-Post on infarct-size, apoptosis and pro-angiogenetic factors were studied in isolated hearts of spontaneously hypertensive rats (SHR), which underwent the following protocols: (a) 30-min ischemia and 120-min reperfusion (I/R); (b) 30-min ischemia and 20-min reperfusion (I/R-short), both with and without CST-Post (75 nM for 20-min at the beginning of reperfusion). In unprotected Wistar-Kyoto hearts, used as normal counterpart, infarct-size resulted smaller than in SHR. CST-Post reduced significantly infarct-size and improved post-ischemic cardiac function in both strains. After 20-min reperfusion, CST-Post induced S-nitrosylation of calcium channels and phosphorylation of RISK-pathway in WKY and SHR hearts. Yet specific inhibitors of the RISK pathway blocked the CST-Post protective effects against infarct in the 120-min reperfusion groups. Moreover, apoptosis (evaluated by TUNEL, ARC and cleaved caspase) was reduced by CST-Post. Importantly, CST-Post increased expression of pro-angiogenetic factors (i.e., HIF-1α and eNOS expression) after two-hour reperfusion.
conclusionsCST-Post limits reperfusion damages and reverses the hypertension-induced increase of I/R susceptibility. Moreover, CST-Post triggers antiapoptotic and pro-angiogenetic factors suggesting that CST-Post can be used as an anti-maladaptive remodeling treatment.
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