The synthesis and secretion of cortisol are controlled by the hypothalamic–pituitary–adrenal axis. Cortisol exhibits a proper 24-h circadian rhythm that affects the brain, the autonomic nervous system, the heart, and the vasculature that prepares the cardiovascular system for optimal function during these anticipated behavioral cycles. A literature search was conducted using databases such as Google Scholar, PubMed, and Scopus. Relevant search terms included “circadian rhythm and cardiovascular”, “cortisol”, “cortisol and acute coronary syndrome”, “cortisol and arrhythmias”, “cortisol and sudden cardiac death”, “cortisol and stroke”, and “cardioprotective agents”. A total of 120 articles were obtained on the basis of the above search. Lower levels of cortisol were seen at the beginning of sleep, while there was a rise towards the end of sleep, with the highest level reached at the moment the individual wakes up. In the present review, we discuss the role of 11β-hydroxysteroid dehydrogenase (11β-HSD1), which is a novel molecular target of interest for treating metabolic syndrome and type-2 diabetes mellitus. 11β-HSD1 is the major determinant of cortisol excess, and its inhibition alleviates metabolic abnormalities. The present review highlights the role of cortisol, which controls the circadian rhythm, and describes its effect on the cardiovascular system. The review provides a platform for future potential cardioprotective therapeutic agents.
Periodontitis is a chronic inflammatory disease of the gums. The incidence of periodontitis is increasing all over the world. In patients with periodontitis, there is gradual destruction of the periodontal ligament and the alveolar bone, and later, in advanced stages, there is tooth loss. Different microorganisms, the host’s immune response, and various environmental factors interact in the progression of this chronic inflammatory disease. In the present review, we discuss the epidemiology, clinical features, diagnosis, and complications of periodontitis. We also discuss the association of chronic inflammation found in periodontitis with various other systemic diseases, which include cardiovascular, respiratory, diabetes, Alzheimer’s, cancer, adverse pregnancy, and multiple myeloma, and also highlight microbial carcinogenesis and the microRNAs involved. The latest updates on the molecular mechanism, possible biomarkers, and treatment procedures may be beneficial for diagnostic and therapeutic purposes.
N-methyl-D-aspartate receptors (NMDAR) are critically involved in the pathogenesis of Alzheimer's disease (AD). Acting as an open-channel blocker, the anti-AD drug memantine preferentially targets NMDAR overactivation, which has been proposed to trigger neurotoxic events mediated by amyloid β peptide (Aβ) and oxidative stress. In this study, we applied a multifunctional approach by conjugating memantine to ferulic acid, which is known to protect the brain from Aβ neurotoxicity and neuronal death caused by ROS.The most interesting compound (7) behaved, like memantine, as a voltage-dependent antagonist of NMDAR (IC 50 = 6.9 µM). In addition, at 10 µM concentration, 7 exerted antioxidant properties both directly and indirectly through the activation of the Nrf-2 pathway in SH-SY5Y cells. At the same concentration, differently from the parent compounds memantine and ferulic acid alone, it was able to modulate Aβ production, as revealed by the observed increase of the non-amyloidogenic sAPPα in H4-sw cells. These findings suggest that compound 7 may represent a promising tool for investigating NMDAR-mediated neurotoxic events involving Aβ burden and oxidative damage.
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