ArticleCardiorenal medicine2012
Regulation of Overnutrition-Induced Cardiac Inflammatory Mechanisms.
Article in Cardiorenal medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Inhibition of eNOS Partially Blunts the Beneficial Effects of Nebivolol on Angiotensin II-Induced Signaling in H9c2 Cardiomyoblasts.Current issues in molecular biology · 2022Article
- miR-208a in Cardiac Hypertrophy and Remodeling.Frontiers in cardiovascular medicine · 2021Review
- Potential roles of mediator Complex Subunit 13 in Cardiac Diseases.International journal of biological sciences · 2021Review
- Differential Regulation of Cardiac Function and Intracardiac Cytokines by Rapamycin in Healthy and Diabetic Rats.Oxidative medicine and cellular longevity · 2017Article
- Regulation of cardiac miR-208a, an inducer of obesity, by rapamycin and nebivolol.Obesity (Silver Spring, Md.) · 2015Article
- The two faces of miR-29.Journal of cardiovascular medicine (Hagerstown, Md.) · 2015Review
- Mineralocorticoid receptor blockade prevents Western diet-induced diastolic dysfunction in female mice.American journal of physiology. Heart and circulatory physiology · 2015Article
- Mitochondrial functional impairment in response to environmental toxins in the cardiorenal metabolic syndrome.Archives of toxicology · 2015Review
- Article
- Overnutrition, mTOR signaling, and cardiovascular diseases.American journal of physiology. Regulatory, integrative and comparative physiology · 2014Review
- Fructose and uric acid: is there a role in endothelial function?Current hypertension reports · 2014Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 3 countries.
Funding
Abstract
backgroundUnlike conventional β-blockers, nebivolol, a third-generation β-adrenergic receptor blocker with vasodilator properties, promotes insulin sensitivity. Objective: The objective of this study was to determine whether nebivolol regulates overnutrition-induced activation of cardiac nutrient sensor kinases and inflammatory signaling.
methodsYoung Zucker obese (ZO) rats, a rodent model for overnutrition, and age-matched Zucker lean rats were treated with nebivolol (10 mg/kg/day; 21 days) and cardiac function was monitored by echocardiography and pressure volume loop analysis. Activation status of nutrient sensor serine/threonine kinases mammalian target for rapamycin (mTOR), and p70 S6kinase (S6K1) and S6K1-substrate RPS6, inflammatory marker Janus kinase 2 (Jak2) and its substrate STAT1, and energy sensor AMP-dependent kinase (AMPK) were monitored by determining phosphorylation status of pSer(2448) of mTOR, pThr(389) of S6K1, pSer(235/236) of RPS6, pTyr(1007/1008) of Jak2, pTyr(701) of STAT1, and pThr(172) of AMPK, respectively.
resultsNebivolol reduced weight and improved cardiac function of ZO rats as shown by improvements in the myocardial performance index and a decrease in the diastolic parameter tau (τ), the time constant of isovolumic relaxation. Nebivolol also attenuated excessive activation of the nutrient sensor kinases mTOR and S6K1 and their substrate RPS6 as well as the inflammatory marker Jak2 and substrate STAT1 in ZO myocardium (p < 0.05). Moreover, nebivolol reversed suppression of the energy sensor kinase AMPK in ZO hearts (p < 0.05).
conclusionWe report for the first time that nebivolol regulates overnutrition-induced activation of cardiac mTOR and Jak/STAT signaling and reverses suppression of AMPK. Since it also suppresses weight gain, nebivolol appears effective in the treatment of overnutrition-related cardiac inflammation and diastolic dysfunction.
Identifiers
What OpenQuestion holds
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.