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http://dx.doi.org/10.1152/ajplegacy.1962.202.2.364 | DOI Listing |
J Cell Mol Med
January 2025
Department of Nephrology, Yi Ji Shan Hospital Affiliated to Wan Nan Medical College, Wuhu, Anhui, China.
Renal fibrosis (RF) is a crucial pathological factor in the progression of chronic kidney disease (CKD) to end-stage renal failure, and accurate and noninvasive assays to monitor the progression of renal fibrosis are needed. Circular RNAs (circRNAs) are noncoding RNAs that can be used as diagnostic biomarkers and therapeutic targets for human diseases. In this study, we analysed the expression of hsa_circ_0008925 in human urinary renal tubular cells and investigated its role in renal fibrosis.
View Article and Find Full Text PDFJ Am Heart Assoc
January 2025
Division of Cardiovascular Science, Faculty of Biology, Medicine and Health The University of Manchester Manchester UK.
Background: Heart failure with preserved ejection fraction (HFpEF) is linked to prolonged endoplasmic reticulum (ER) stress. P21-activated kinase 2 (Pak2) facilitates a protective ER stress response. This study explores the mechanism and role of Pak2 in HFpEF pathology.
View Article and Find Full Text PDFBiomolecules
November 2024
Departments of Pediatrics, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul 06229, Republic of Korea.
Mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome is a complex mitochondrial disorder characterized by a wide range of systemic manifestations. Key clinical features include recurrent stroke-like episodes, seizures, lactic acidosis, muscle weakness, exercise intolerance, sensorineural hearing loss, diabetes, and progressive neurological decline. MELAS is most commonly associated with mutations in mitochondrial DNA, particularly the m.
View Article and Find Full Text PDFEMBO J
January 2025
Newcastle University Biosciences Institute (NUBI), Central Parkway, Newcastle University, NE1 3BZ, Newcastle upon Tyne, UK.
The cellular concentrations of splicing factors (SFs) are critical for controlling alternative splicing. Most serine and arginine-enriched (SR) protein SFs regulate their own concentration via a homeostatic feedback mechanism that involves regulation of inclusion of non-coding 'poison exons' (PEs) that target transcripts for nonsense-mediated decay. The importance of SR protein PE splicing during animal development is largely unknown despite PE ultra-conservation across animal genomes.
View Article and Find Full Text PDFBiochem Pharmacol
December 2024
Department of Molecular, Cellular, and Biomedical Sciences, Sophie Davis School of Biomedical Education, City University of New York School of Medicine, New York, NY, USA; Graduate Program in Biology, City University of New York Graduate Center, New York 10091, USA.
One possible reason for failure in achieving optimal glycemic control in patients with type 2 diabetes (T2D) is that less attention has been paid to the brain, a fundamental player in glucose homeostasis, that consumes about 25% of total glucose utilization. In addition, animal and human studies indicate that nitric oxide (NO) is a critical player in glucose metabolism. NO synthesis from L-arginine is lower in patients with T2D, and endothelial NO synthase (eNOS)-derived NO bioavailability is lower in T2D.
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