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Overexpression of FTO alleviates traumatic brain injury induced posttraumatic epilepsy by upregulating NR4A2 expression via m6A demethylation.
Funct Integr Genomics
January 2025
Department of Radiology, The Second Xiangya Hospital of Central South University, No. 139, Renmin Middle Road, Furong District, Changsha City, Hunan Province, 410011, China.
Post-traumatic epilepsy (PTE) is a debilitating chronic outcome of traumatic brain injury (TBI). Although FTO has been reported as a possible intervention target of TBI, its precise roles in the PTE remain incompletely understood. Here we used mild or serious mice TBI model to probe the role and molecular mechanism of FTO in PTE.
View Article and Find Full Text PDFLong-term hemodynamic responses and reverse remodeling after pharmacotherapy in HFpEF versus HFrEF: a systematic review and meta-analysis.
Am J Physiol Heart Circ Physiol
January 2025
Amsterdam University Medical Centers, Vrije Universiteit Amsterdam, Department of Cardiology, Amsterdam, The Netherlands.
The acute response to therapeutic afterload reduction differs between heart failure with preserved (HFpEF) versus reduced ejection fraction (HFrEF), with larger left ventricular (LV) stroke work augmentation in HFrEF compared to HFpEF. This may (partially) explain the neutral effect of HFrEF-medication in HFpEF. It is unclear whether such differences in hemodynamic response persist and/or differentially trigger reverse remodeling in case of long-term afterload reduction.
View Article and Find Full Text PDFGeneration of human and murine exhausted CD8 T cells in vitro.
Methods Cell Biol
January 2025
Department of Immunology and Oncology, Centro Nacional de Biotecnología (CNB/CSIC), Madrid, Spain. Electronic address:
T cell exhaustion is a state of dysfunction that can occur due to persistent exposure to antigens, such as in the tumor microenvironment. The progressive loss of effector functions in exhausted T cells can lead to resistance to immune checkpoint inhibitors and adoptive cell immunotherapies. Improving our understanding of the exhaustion process is thus crucial for optimizing the clinical outcomes of immunotherapy.
View Article and Find Full Text PDFTGR5 attenuates DOCA-salt hypertension through regulating histone H3K4 methylation of ENaC in the kidney.
Metabolism
January 2025
Institute of Hypertension, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China; Department of Pathophysiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China. Electronic address:
Epithelial sodium channel (ENaC), located in the collecting duct principal cells of the kidney, is responsible for the reabsorption of sodium and plays a critical role in the regulation of extracellular fluid volume and consequently blood pressure. The G protein-coupled bile acid receptor (TGR5) is a membrane receptor mediating effects of bile acid and is implicated in kidney diseases. The current study aims to investigate whether TGR5 activation in the kidney regulated ENaC expression and potential mechanism.
View Article and Find Full Text PDFOral glucose-responsive nanoparticles loaded with artemisinin induce pancreatic β-cell regeneration for the treatment of type 2 diabetes.
J Colloid Interface Sci
January 2025
School of Life Science, South China Normal University, Guangzhou 510631 China; Guangzhou Key Laboratory of Spectral Analysis and Functional Probes, College of Biophotonics, South China Normal University, Guangzhou 510631 China; South China Normal University-Panyu Central Hospital Joint Laboratory of Translational Medical Research, Panyu Central Hospital, Guangzhou 511400 China. Electronic address:
Type 2 diabetes (T2D) is a chronic disease characterized by long-term insulin resistance (IR) and pancreatic β-cell dysfunction. Conventional T2D medication ignores pancreatic β-cell damage. In this study, we designed an oral glucose-responsive nanoparticle for pancreatic β-cell regeneration and treatment of T2D.
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