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Hypertension is the leading risk factor for global mortality and morbidity and those with hypertension are more likely to develop severe symptoms in cardiovascular and cerebrovascular system, which is closely related to abnormal renin-angiotensin system and elabela/apelin-apelin receptor (APJ) axis. The elabela/apelin-APJ axis exerts essential roles in regulating blood pressure levels, vascular tone, and cardiovascular dysfunction in hypertension by counterbalancing the action of the angiotensin II/angiotensin II type 1 receptor axis and enhancing the endothelial nitric oxide (NO) synthase/NO signaling. Furthermore, the elabela/apelin-APJ axis demonstrates beneficial effects in cardiovascular physiology and pathophysiology, including angiogenesis, cellular proliferation, fibrosis, apoptosis, oxidative stress, and cardiovascular remodeling and dysfunction during hypertension. More importantly, effects of the elabela/apelin-APJ axis on vascular tone may depend upon blood vessel type or various pathological conditions. Intriguingly, the broad distribution of elabela/apelin and alternative isoforms implicates its distinct functions in diverse cardiac and vascular cells and tissue types. Finally, both loss-of-function and gain-of-function approaches have defined critical roles of the elabela/apelin-APJ axis in reducing the development and severity of hypertensive diseases. Thus, targeting the elabela/ apelin-APJ axis has emerged as a pre-warning biomarker and a novel therapeutic approach against progression of hypertension, and an increased understanding of cardiovascular actions of the elabela/apelin-APJ axis will help to develop effective interventions for hypertension. In this review, we focus on the physiology and biochemistry, diverse actions, and underlying mechanisms of the elabela/apelin-APJ axis, highlighting its role in hypertension and hypertensive cardiovascular injury and dysfunction, with a view to provide a prospective strategy for hypertensive disease therapy.
Hypertension is the leading risk factor for global mortality and morbidity and those with hypertension are more likely to develop severe symptoms in cardiovascular and cerebrovascular system, which is closely related to abnormal renin-angiotensin system and elabela/apelin-apelin receptor (APJ) axis. The elabela/apelin-APJ axis exerts essential roles in regulating blood pressure levels, vascular tone, and cardiovascular dysfunction in hypertension by counterbalancing the action of the angiotensin II/angiotensin II type 1 receptor axis and enhancing the endothelial nitric oxide (NO) synthase/NO signaling. Furthermore, the elabela/apelin-APJ axis demonstrates beneficial effects in cardiovascular physiology and pathophysiology, including angiogenesis, cellular proliferation, fibrosis, apoptosis, oxidative stress, and cardiovascular remodeling and dysfunction during hypertension. More importantly, effects of the elabela/apelin-APJ axis on vascular tone may depend upon blood vessel type or various pathological conditions. Intriguingly, the broad distribution of elabela/apelin and alternative isoforms implicates its distinct functions in diverse cardiac and vascular cells and tissue types. Finally, both loss-of-function and gain-of-function approaches have defined critical roles of the elabela/apelin-APJ axis in reducing the development and severity of hypertensive diseases. Thus, targeting the elabela/ apelin-APJ axis has emerged as a pre-warning biomarker and a novel therapeutic approach against progression of hypertension, and an increased understanding of cardiovascular actions of the elabela/apelin-APJ axis will help to develop effective interventions for hypertension. In this review, we focus on the physiology and biochemistry, diverse actions, and underlying mechanisms of the elabela/apelin-APJ axis, highlighting its role in hypertension and hypertensive cardiovascular injury and dysfunction, with a view to provide a prospective strategy for hypertensive disease therapy.
Ziel dieser Studie war die Evaluation von Patienten, die eine transfemorale oder eine transapikale TAVI erhalten haben, in Bezug auf ihre Mortalitätsprädiktoren und ihre Langzeit-Mortalität. Methoden Untersucht wurden Patienten mit einer minimalen FU-Zeit von sechs Jahren, welche im Zeitraum von 2006 – 2014 eine TAVI im Herzkatheterlabor des Universitätsklinikums in Frankfurt erhalten haben. Das Patientenkollektiv wurde basierend auf dem Zugangsweg (transfemoral oder transapikal) analysiert. Ergebnisse Insgesamt wurden 679 Patienten in die Studie eingeschlossen. 408 Patienten (59,82 %) bekamen eine transfemorale TAVI und 271 Patienten (39,74 %) bekamen eine transapikale TAVI. Der durchschnittliche STS-Score betrug in der transfemoralen Gruppe 4,21 ± 2,4 % und in der transapikalen Gruppe 4,19 ± 2,7 %. Die Mortalität war nach 30 Tagen (15,8 % transapikal versus 8,2 % transfemoral, p = 0,00) sowie im Langzeit-FU (79,5 % transapikal versus 68,3 % transfemoral, p = 0,00) signifikant höher in der transapikalen Gruppe. Viele postinterventionelle Komplikationen waren häufiger in der transfemoralen Gruppe. Postinterventionelle Schrittmacherimplantationen (15,7 % versus 4,1 %, p = 0,00), große und kleine vaskuläre Komplikationen (5,1 % versus 1,1 %, p = 0,01) sowie große und kleine zerebrovaskuläre Insulte (31,8 % versus 9,1 %, p = 0,00) kamen in der transfemoralen Gruppe signifikant häufiger vor. Allerdings war der transfemorale Zugangsweg mit einer besseren Überlebensrate assoziiert (Log Rank Test p = 0,01 und HR 1,33 (1,04 – 1,71), p = 0,03). Patienten mit einem hohen STS-Score (HR 1,09 (1,03 – 1,15), p = 0,00), einem vorbestehenden Diabetes Mellitus (HR 0,75 (0,58 – 0,97), p = 0,03) sowie großen Gefäßkomplikationen (HR 0,60 (0,37 – 0,99), p = 0,04) korrelieren mit einem schlechteren Langzeit-Überleben. Zusammenfassung Für den kathetergestützten Aortenklappenersatz weisen beide Zugangswege spezifische Risiken auf, daher sollte die individuell beste Variante für jeden Patienten ausgewählt werden.
Objective: This study aimed to investigate the effects of serum levels of apelin and CD40L on major adverse cardiovascular events (MACEs) after percutaneous coronary intervention (PCI). Methods: A case–control study was conducted to select patients undergoing PCI in our hospital from June 2020 to June 2022. Patients were divided into the occurrence group and the non-occurrence group according to whether MACEs occurred during the 12-month follow-up after surgery. Enzyme-linked immunosorbent assay was used to detect the expression levels of serum apelin and CD40L in the two groups, and the correlation between the expression of apelin and CD40L and prognosis was analyzed. Logistic regression analysis was performed on the indicators with differences to analyze the influencing factors of the prognosis of PCI. Results: Compared with the non-occurrence group, the occurrence group had a significantly lower level of apelin and a significantly higher level of CD40L (p < 0.001). Apelin was negatively correlated with the occurrence of MACEs after PCI (r = –0.583, p < 0.001), and CD40L was positively correlated with the occurrence of MACEs after PCI (r = 0.569, p < 0.001). Logistic regression analysis showed that apelin was a protective factor for MACEs after PCI (odds ratio (OR) = 0.248, p < 0.001); CD40L, age, hypertension, and the number of diseased vessels were risk factors for MACEs after PCI (OR = 8.684, 0.018, 0.003, 0.020, p < 0.05). The area under curve (AUC) of apelin combined with CD40L was large, and the predictive value was higher than that of apelin and CD40L alone (AUC values were 0.956, 0.857, 0.905, p < 0.001; p < 0.001; p < 0.001). Conclusions: This study showed that the levels of apelin and CD40L were correlated with MACEs after PCI. Clinicians should pay close attention to the levels of apelin and CD40L in patients after PCI and be alert to the occurrence of MACEs.
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