Abstract: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-… Show more
“…In the study of Alqaderi et al, levels of leptin and VEGF in saliva were found not to be good predictors of obesity or hyperglycemia in adolescents 123 . Our own studies have shown that cardiac rehabilitation can decrease serum leptin and HIF‐1A levels in patients who have undergone acute coronary syndrome 124 …”
Section: Resultsmentioning
confidence: 68%
“…[112][113][114][115] Studies of patients with obesity have confirmed the genetic or epigenetic aspect of leptin-VEGF crosstalk, pointing to the role of obesity-dependent leptin gene regulation. [104][105][106][107] These studies have also revealed that leptin-VEGF crosstalk is a complicated network, involving leptin canonical and noncanonical signaling pathways, HIF-1A, and NfkB as the core, 97,124,136 with a range of substances (including adiponectin, visfatin, ghrelin, IL-6, insulin, cholesterol, LDL, triglycerides, ApoB, trimethylamine N-oxide, and NO) acting as accompanying, modifying, and disrupting factors. [99][100][101] In female patients with excess body mass and related disorders, leptin-VEGF crosstalk may be involved in PCOS, adverse pregnancy outcome, 129 and preeclampsia.…”
Section: Discussionmentioning
confidence: 99%
“…123 Our own studies have shown that cardiac rehabilitation can decrease serum leptin and HIF-1A levels in patients who have undergone acute coronary syndrome. 124 Research in obstetrics and gynecology investigating the associations between leptin and VEGF in relation to excess body mass and related disorders have also been performed. In patients with polycystic ovary syndrome (PCOS) with obesity, the serum leptin level is lower than in normo-ovulatory women with obesity, whereas VEGF levels are almost four times higher.…”
Summary
By 2030, it is expected that a billion people will have suffer from obesity. Adipose tissue synthesizes leptin, an adipokine that affects cardiovascular risk. Leptin intensifies the synthesis of vascular endothelial growth factor (VEGF). Our study reviews recent reports on leptin–VEGF crosstalk in obesity and related disorders. PubMed, Web of Science, Scopus, and Google Scholar were searched. One hundred and one articles involving human, animal, and in vitro research were included. In vitro studies show the crucial role of interaction between endothelial cells and adipocytes and hypoxia as a factor that intensifies leptin's effects on VEGF. Leptin–VEGF crosstalk promotes the progression of cancer. The animal research reveal that a high‐fat diet enhances leptin and VEGF crosstalk. Genetic and epigenetic mechanisms and procreator‐offspring programming may be involved in leptin–VEGF crosstalk. Some female‐specific characteristics of leptin–VEGF relation in obesity were observed. The human studies have shown that increased leptin and VEGF synthesis and leptin–VEGF crosstalk are factors linking obesity with elevated cardiovascular risk. The studies of the last 10 years documented a range of significant aspects of leptin–VEGF crosstalk specific for obesity and related disorders, shedding new light on the link between obesity and increased cardiovascular risk.
“…In the study of Alqaderi et al, levels of leptin and VEGF in saliva were found not to be good predictors of obesity or hyperglycemia in adolescents 123 . Our own studies have shown that cardiac rehabilitation can decrease serum leptin and HIF‐1A levels in patients who have undergone acute coronary syndrome 124 …”
Section: Resultsmentioning
confidence: 68%
“…[112][113][114][115] Studies of patients with obesity have confirmed the genetic or epigenetic aspect of leptin-VEGF crosstalk, pointing to the role of obesity-dependent leptin gene regulation. [104][105][106][107] These studies have also revealed that leptin-VEGF crosstalk is a complicated network, involving leptin canonical and noncanonical signaling pathways, HIF-1A, and NfkB as the core, 97,124,136 with a range of substances (including adiponectin, visfatin, ghrelin, IL-6, insulin, cholesterol, LDL, triglycerides, ApoB, trimethylamine N-oxide, and NO) acting as accompanying, modifying, and disrupting factors. [99][100][101] In female patients with excess body mass and related disorders, leptin-VEGF crosstalk may be involved in PCOS, adverse pregnancy outcome, 129 and preeclampsia.…”
Section: Discussionmentioning
confidence: 99%
“…123 Our own studies have shown that cardiac rehabilitation can decrease serum leptin and HIF-1A levels in patients who have undergone acute coronary syndrome. 124 Research in obstetrics and gynecology investigating the associations between leptin and VEGF in relation to excess body mass and related disorders have also been performed. In patients with polycystic ovary syndrome (PCOS) with obesity, the serum leptin level is lower than in normo-ovulatory women with obesity, whereas VEGF levels are almost four times higher.…”
Summary
By 2030, it is expected that a billion people will have suffer from obesity. Adipose tissue synthesizes leptin, an adipokine that affects cardiovascular risk. Leptin intensifies the synthesis of vascular endothelial growth factor (VEGF). Our study reviews recent reports on leptin–VEGF crosstalk in obesity and related disorders. PubMed, Web of Science, Scopus, and Google Scholar were searched. One hundred and one articles involving human, animal, and in vitro research were included. In vitro studies show the crucial role of interaction between endothelial cells and adipocytes and hypoxia as a factor that intensifies leptin's effects on VEGF. Leptin–VEGF crosstalk promotes the progression of cancer. The animal research reveal that a high‐fat diet enhances leptin and VEGF crosstalk. Genetic and epigenetic mechanisms and procreator‐offspring programming may be involved in leptin–VEGF crosstalk. Some female‐specific characteristics of leptin–VEGF relation in obesity were observed. The human studies have shown that increased leptin and VEGF synthesis and leptin–VEGF crosstalk are factors linking obesity with elevated cardiovascular risk. The studies of the last 10 years documented a range of significant aspects of leptin–VEGF crosstalk specific for obesity and related disorders, shedding new light on the link between obesity and increased cardiovascular risk.
“…All these studies proved that PWV is one of the key factors influencing cardiovascular risk in patients with subclinical MetS. Recently, Skrypnik et al indicated that the implementation of the cardiac rehabilitation programme can lead to a decrease in serum leptin levels [14], which can influence arterial stiffness [15].…”
Introduction: Carotid-femoral pulse wave velocity reflecting aortic stiffness could be used as an independent predictor of future cardiovascular events for an individual with metabolic syndrome. However, the routine use of carotid-femoral pulse wave velocity is suboptimized in clinical practice. We report a case of metabolic syndrome with increased carotid-femoral pulse wave velocity and subsequently developed myocardial infarction and sudden cardiac arrest. Case presentation: A Polish man of an age between 40 and 50 years previously diagnosed with metabolic syndrome with essential hypertension, obesity, dyslipidaemia, and impaired glucose level. He developed myocardial infarction, ventricular fibrillation, and was successfully resuscitated with defibrillation. The patient showed high–normal traditional cardiovascular risk factors but an increased carotid-femoral pulse wave velocity. The increased carotid-femoral pulse wave velocity is associated with an increased arterial stiffness, which altered the myocardial perfusion and induced the anterior-lateral ST elevation myocardial infarction. The patient actively participated and completed the phase II cardiac rehabilitation programme. To the best of our knowledge, there have been few studies on carotid-femoral pulse wave velocity screening for patients with metabolic syndrome. Pulse wave velocity screening by a physician appears to be helpful in identifying the potential high-risk population with borderline traditional cardiovascular risk factors. Conclusion: This trajectory highlights the clinical relevance of using carotid-femoral pulse wave velocity as an adjunct marker to assess the risk of cardiovascular event for patients with metabolic syndrome.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.