PreprintArticleVersion 1Preserved in Portico This version is not peer-reviewed
Hyperleptinemia Results in Systemic Inflammation and the Exacerbation of Ischemia-Reperfusion Myocardial Injury: The Involvement of the JAK/STAT Pathway
Version 1
: Received: 31 July 2021 / Approved: 2 August 2021 / Online: 2 August 2021 (11:24:57 CEST)
How to cite:
Polyakova, E.A.; Mikhaylov, E.N.; Galagudza, M.M.; Shlyakhto, E.V. Hyperleptinemia Results in Systemic Inflammation and the Exacerbation of Ischemia-Reperfusion Myocardial Injury: The Involvement of the JAK/STAT Pathway. Preprints2021, 2021080019. https://doi.org/10.20944/preprints202108.0019.v1
Polyakova, E.A.; Mikhaylov, E.N.; Galagudza, M.M.; Shlyakhto, E.V. Hyperleptinemia Results in Systemic Inflammation and the Exacerbation of Ischemia-Reperfusion Myocardial Injury: The Involvement of the JAK/STAT Pathway. Preprints 2021, 2021080019. https://doi.org/10.20944/preprints202108.0019.v1
Polyakova, E.A.; Mikhaylov, E.N.; Galagudza, M.M.; Shlyakhto, E.V. Hyperleptinemia Results in Systemic Inflammation and the Exacerbation of Ischemia-Reperfusion Myocardial Injury: The Involvement of the JAK/STAT Pathway. Preprints2021, 2021080019. https://doi.org/10.20944/preprints202108.0019.v1
APA Style
Polyakova, E.A., Mikhaylov, E.N., Galagudza, M.M., & Shlyakhto, E.V. (2021). Hyperleptinemia Results in Systemic Inflammation and the Exacerbation of Ischemia-Reperfusion Myocardial Injury: The Involvement of the JAK/STAT Pathway. Preprints. https://doi.org/10.20944/preprints202108.0019.v1
Chicago/Turabian Style
Polyakova, E.A., Mikhail M. Galagudza and Evgeny V. Shlyakhto. 2021 "Hyperleptinemia Results in Systemic Inflammation and the Exacerbation of Ischemia-Reperfusion Myocardial Injury: The Involvement of the JAK/STAT Pathway" Preprints. https://doi.org/10.20944/preprints202108.0019.v1
Abstract
Hyperleptinemia potentiates the effects of many atherogenic factors, such as inflammation, platelet aggregation, migration, hypertrophy, proliferation of vascular smooth muscle cells, and endothelial cell dysfunction. The present study analysed the effects of long-term hyperleptinemia in an in vivo myocardial ischemia-reperfusion model to demonstrate whether the in vivo deleterious effect also affects cardiac structure and function. Rats by were subcutaneously administered leptin for 8 days to estimate the involvement of the JAK/STAT pathway. Data from 58 male Wistar rats were included in the final analysis. Myocardial infarction (MI) was modelled by the 30-minute ligation of the main left coronary artery followed by 120-minute reperfusion. Hemodynamic measurements, electrocardiography monitoring, echocardiography, myocardial infarct size and area at risk, blood biochemical parameters, leptin, IL-6, TNF-alpha, FGF-21, and cardiomyocyte morphology were measured. Statistical analyses were performed using IBM SPSS Statistics v.26. Seven-day hyperleptinemia in rats led to increased an blood pressure and heart rate, myocardial hypertrophy, impaired LV function, an increased frequency of ischemic arrhythmias, dyslipidaemia, systemic inflammation, and an increased size of induced myocardial infarction. The blockade of the JAK/STAT signalling pathway effectively reversed the negative effects of leptin, including increased blood pressure and total cholesterol.
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
