Cardiac rehabilitation may influence leptin and VEGF A crosstalk in patients after acute coronary syndrome.

Sci Rep

Department of Treatment of Obesity, Metabolic Disorders and Clinical Dietetics, Poznań University of Medical Sciences, Szamarzewskiego St. 82/84, 60-569, Poznan, Poland.

Published: July 2022

Leptin, a well-proven cardiovascular risk factor, influences vascular endothelial growth factor A (VEGF A) synthesis via hypoxia-inducible factor 1 alpha (HIF-1A), nuclear factor kappa-light-chain-enhancer of activated B cells (NfkB) and NILCO (Notch, interleukin 1 [IL1] and leptin cross-talk outcome) pathways. This study aimed to investigate the influence of cardiac rehabilitation (CR) on HIF-1A, NfkB and NILCO dependent leptin and VEGF A cross-talk in patients after acute coronary syndrome (ACS). Fifty post-ACS patients underwent a 2-week CR programme (study group S) and were compared to 50 post-ACS subjects who did not undergo CR (control group K). In group S, at baseline and at completion and in group K once, anthropometric, body composition, blood pressure and heart rate measurements were taken and blood sampling was performed. Serum levels of leptin, VEGF A, VEGF receptor 2 (VEGF R2), HIF-1A, NfkB, interleukin 1-alpha (IL1-alpha) and Notch 1 were determined. In group S, serum VEGF A levels increased while leptin, HIF-1A and VEGF R2 levels decreased and completion but not baseline serum leptin correlated positively with serum VEGF A. Also, serum completion VEGF A correlated positively with NfkB and HIF-1A in group S. Correlation analysis in group S confirmed the significant role of the NILCO pathway in the regulation of VEGF A serum levels mediated by HIF-1A and NfkB. CR may induce the predomination of the NILCO pathway interacting with HIF-1A and NfkB over leptin canonical and non-canonical signalling pathways in the leptin influence on VEGF A in post-ACS patients.Trial registration: ClinicalTrials.gov ID: NCT03935438. The CARDIO-REH randomised study.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9276756PMC
http://dx.doi.org/10.1038/s41598-022-16053-1DOI Listing

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