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| http://dx.doi.org/10.1161/CIRCRESAHA.120.317624 | DOI Listing |
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Sex-Specific Differences in the Pathophysiology of Hypertension.
Biomolecules
January 2025
Department of Physiology and Pathophysiology, St. Boniface Hospital Albrechtsen Research Centre, Institute of Cardiovascular Sciences, Rady College of Medicine, Max Rady Faculty of Health Sciences, University of Manitoba, Rm. 3042, 351 Taché Avenue, Winnipeg, MB R2H 2A6, Canada.
Hypertension is one of the most common comorbidities in cardiometabolic diseases, affecting nearly one third of adults. As a result, its pathophysiological mechanisms have been studied extensively and are focused around pressure natriuresis, the renin-angiotensin system (RAS), the sympathetic nervous system, oxidative stress, and endothelial dysfunction. Additionally, hypertension secondary to other underlying etiologies also exists.
View Article and Find Full Text PDFThe renin-angiotensin-aldosterone system and salt sensitivity of blood pressure offer new insights in obesity phenotypes.
Obesity (Silver Spring)
January 2025
Division of Endocrinology, Diabetes and Hypertension, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Objective: Individuals who have metabolically healthy overweight/obesity (MHOO) do not have cardiometabolic complications despite an elevated BMI. Renin-angiotensin-aldosterone system (RAAS) activation and salt sensitivity of blood pressure (SSBP) are cardiovascular disease (CVD) risks, which are increased in individuals with higher BMI values. Little is known about the differences in RAAS activation and SSBP between MHOO and metabolically unhealthy overweight/obesity (MUOO) phenotypes.
View Article and Find Full Text PDFPhosphoproteomics for studying signaling pathways evoked by hormones of the renin-angiotensin system: A source of untapped potential.
Acta Physiol (Oxf)
February 2025
Department of Molecular Medicine, Cardiovascular and Renal Research Unit, University of Southern Denmark, Odense M, Denmark.
The Renin-Angiotensin System (RAS) is a complex neuroendocrine system consisting of a single precursor protein, angiotensinogen (AGT), which is processed into various peptide hormones, including the angiotensins [Ang I, Ang II, Ang III, Ang IV, Ang-(1-9), Ang-(1-7), Ang-(1-5), etc] and Alamandine-related peptides [Ang A, Alamandine, Ala-(1-5)], through intricate enzymatic pathways. Functionally, the RAS is divided into two axes with opposing effects: the classical axis, primarily consisting of Ang II acting through the AT receptor (ATR), and in contrast the protective axis, which includes the receptors Mas, ATR and MrgD and their respective ligands. A key area of RAS research is to gain a better understanding how signaling cascades elicited by these receptors lead to either "classical" or "protective" effects, as imbalances between the two axes can contribute to disease.
View Article and Find Full Text PDFAnti-inflammatory effect of Angiotensin 1-7 in white adipose tissue.
Adipocyte
December 2025
Department of Pediatrics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Obesity is a global health concern that promotes chronic low-grade inflammation, leading to insulin resistance, a key factor in many metabolic diseases. Angiotensin 1-7 (Ang 1-7), a component of the renin-angiotensin system (RAS), exhibits anti-inflammatory effects in obesity and related disorders, though its mechanisms remain unclear. In this study, we examined the effect of Ang 1-7 on inflammation of white adipose tissue (WAT) in dietary-induced obese mice.
View Article and Find Full Text PDFAtrial Fibrosis in Atrial Fibrillation: Mechanistic Insights, Diagnostic Challenges, and Emerging Therapeutic Targets.
Int J Mol Sci
December 2024
Second Department of Cardiology, Hippokration General Hospital, Aristotle University of Thessaloniki, 54642 Thessaloniki, Greece.
Atrial fibrosis is a hallmark of atrial cardiomyopathy and plays a pivotal role in the pathogenesis of atrial fibrillation (AF), contributing to its onset and progression. The mechanisms underlying atrial fibrosis are multifaceted, involving stretch-induced fibroblast activation, oxidative stress, inflammation, and coagulation pathways. Variations in fibrosis types-reactive and replacement fibrosis-are influenced by patient-specific factors such as age, sex, and comorbidities, complicating therapeutic approaches.
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