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Function: insertAPISummary
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Uremic cardiomyopathy is characterized by diastolic dysfunction, left ventricular hypertrophy (LVH), and fibrosis. Dysregulation of the kisspeptin receptor (KISS1R)-mediated pathways are associated with the development of fibrosis in cancerous diseases. Here, we investigated the effects of the KISS1R antagonist peptide-234 (P234) on the development of uremic cardiomyopathy. Male Wistar rats (300-350 g) were randomized into four groups: (i) Sham, (ii) chronic kidney disease (CKD) induced by 5/6 nephrectomy, (iii) CKD treated with a lower dose of P234 (ip. 13 µg/day), (iv) CKD treated with a higher dose of P234 (ip. 26 µg/day). Treatments were administered daily from week 3 for 10 days. At week 13, the P234 administration did not influence the creatinine clearance and urinary protein excretion. However, the higher dose of P234 led to reduced anterior and posterior wall thicknesses, more severe interstitial fibrosis, and overexpression of genes associated with left ventricular remodeling (Ctgf, Tgfb, Col3a1, Mmp9), stretch (Nppa), and apoptosis (Bax, Bcl2, Casp7) compared to the CKD group. In contrast, no significant differences were found in the expressions of apoptosis-associated proteins between the groups. Our results suggest that the higher dose of P234 hastens the development and pathophysiology of uremic cardiomyopathy by activating the fibrotic TGF-β-mediated pathways.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10462750 | PMC |
http://dx.doi.org/10.1038/s41598-023-41037-0 | DOI Listing |
Semin Vasc Surg
December 2024
Division of Vascular Surgery and Endovascular Therapy, Michael E. DeBakey Department of Surgery, Baylor College of Medicine, One Baylor Plaza, BCM 390, Houston TX 77030.
Chronic kidney disease and dialysis-dependent end-stage renal disease are increasing in prevalence in the United States. The costs associated with end-stage renal disease management comprise approximately 1% of the federal government's annual budget. Chronic kidney disease and end-stage renal disease cause significant derangements of the cardiac and vascular system.
View Article and Find Full Text PDFESC Heart Fail
November 2024
Department of Clinical Sciences and Advanced Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Background And Aims: The heart is a metabolic organ rich in mitochondria. The failing heart reprograms to utilize different energy substrates, which increase its oxygen consumption. These adaptive changes contribute to increased oxidative stress.
View Article and Find Full Text PDFEnviron Toxicol
October 2024
Vascular Biology Lab, School of Chemical and Biotechnology, SASTRA Deemed University, Thanjavur, Tamil Nadu, India.
Patients with chronic kidney disease (CKD) frequently develop uremic cardiomyopathy, characterized by mitochondrial dysfunction as one of its pathologically significant mediators. Given that PM specifically targets cardiac mitochondria, exacerbating toxicity, this study addresses the potential alterations in the severity of PM toxicity in the context of CKD conditions. Female Wistar rats were exposed to PM at a concentration of 250 μg/m daily for 3 h for 21 days after which an adenine-induced CKD model was developed.
View Article and Find Full Text PDFFront Immunol
October 2024
Internal Medicine Department, Fatebenefratelli Hospital, Milan, Italy.
Zhonghua Er Ke Za Zhi
October 2024
Pediatric Intensive Care Unit, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health, Beijing 100045, China.
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