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Diagnosis, Severity, and Prognosis from Potential Biomarkers of COVID-19 in Urine: A Review of Clinical and Omics Results.
Metabolites
December 2024
Department of Biochemistry and Molecular Biology and Soil Science and Agricultural Chemistry, University of Alicante, 03690 Alicante, Spain.
The COVID-19 pandemic, caused by the SARS-CoV-2 virus, has spurred an extraordinary scientific effort to better understand the disease's pathophysiology and develop diagnostic and prognostic tools to guide more precise and effective clinical management. Among the biological samples analyzed for biomarker identification, urine stands out due to its low risk of infection, non-invasive collection, and suitability for frequent, large-volume sampling. Integrating data from omics studies with standard biochemical analyses offers a deeper and more comprehensive understanding of COVID-19.
View Article and Find Full Text PDFFasting recovers age-related hypertension in the rats: reset of renal renin-angiotensin system components and klotho.
BMC Nephrol
December 2024
Department of Immunology, Faculty of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Background: The renal renin-angiotensin system (RAS) plays a vital part in the control of blood pressure and is known to be affected by aging. This study aimed to investigate the effects of intermittent fasting on age-related hypertension and the expression of local renal RAS components.
Methods: The Wistar rats were categorized into three main age groups (young, middle aged, and elderly) and three dietary treatment models, including ad libitum feeding (AL), every other day fasting (EOD), and one day per week of fasting (FW).
Bioinformatic characterization of ENPEP, the gene encoding a potential cofactor for SARS-CoV-2 infection.
PLoS One
December 2024
Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland.
Research on SARS-CoV-2, the viral pathogen that causes COVID-19, has identified angiotensin converting enzyme 2 (ACE2) as the primary viral receptor. Several genes that encode viral cofactors, such as TMPRSS2, NRP1, CTSL, and possibly KIM1, have since been discovered. Glutamyl aminopeptidase (APA), encoded by the gene ENPEP, is another cofactor candidate due to similarities in its biological role and high correlation with ACE2 and other human coronavirus receptors, such as aminopeptidase N (APN) and dipeptidyl peptidase 4 (DPP4).
View Article and Find Full Text PDFChenodeoxycholic acid alleviated the cyclosporine-induced nephrotoxicity by decreasing oxidative stress and suppressing renin-angiotensin system through AT2R and ACE2 mRNA upregulation in rats.
J Mol Histol
December 2024
Department of Medical Biochemistry, Istanbul Faculty of Medicine, Istanbul University, Istanbul, Turkey.
Oxidative stress, inflammation and renin-angiotensin system (RAS) activation play an important role in the nephrotoxicity which is caused by the long-term use of the immunosuppressive drug cyclosporine (CsA). This study investigates whether chenodeoxycholic acid (CDCA), an endogenous farnesoid X receptor (FXR) agonist with antioxidant and anti-inflammatory effects, modulates CsA nephrotoxicity. CsA (25 mg/kg/day; s.
View Article and Find Full Text PDFNephro- and Cardiotoxic Effects of Etoricoxib: Insights into Arachidonic Acid Metabolism and Beta-Adrenergic Receptor Expression in Experimental Mice.
Pharmaceuticals (Basel)
October 2024
Department of Physiology, Faculty of Medicine, King Abdulaziz University, Jeddah 21589, Saudi Arabia.
Etoricoxib is a widely used anti-inflammatory drug, but its safety profile concerning cardiovascular and renal health remains inadequately explored. This study aimed to assess the nephro- and cardiotoxic effects of etoricoxib in a murine model, with a focus on its impact on arachidonic acid-metabolizing enzymes and beta-adrenergic receptors associated with drug-induced toxicity. Thirty-five mice were randomly assigned to five groups: control, low-dose etoricoxib, high-dose etoricoxib, low-dose celecoxib, and high-dose celecoxib (a well-known nephro- and cardiotoxic NSAID).
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