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Mechanosensitive Ca channel TRPV1 activated by low-intensity pulsed ultrasound ameliorates acute kidney injury through Notch1-Akt-eNOS signaling.
FASEB J
January 2025
Department of Urology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Acute Kidney Injury (AKI) is a significant medical condition characterized by the abrupt decline in kidney function.Low-intensity pulsed ultrasound (LIPUS), a non-invasive therapeutic technique employing low-intensity acoustic wave pulses, has shown promise in promoting tissue repair and regeneration. A novel LIPUS system was developed and evaluated in rat AKI models, focusing on its effects on glomerular filtration rate (GFR), blood urea nitrogen (BUN), serum creatinine (SCr), and the Notch1-Akt-eNOS signaling pathway.
View Article and Find Full Text PDFBackground: While the formation of β-amyloid plaques and neurofibrillary "tau" tangles are considered hallmarks of AD pathology, therapeutic targeting of these pathways has been unsuccessful, highlighting the necessity to define the underlying molecular mechanisms driving AD progression. Previous studies from our lab demonstrated that mitochondrial calcium (Ca) overload through neuronal ablation of the mitochondrial Na/Ca exchanger (NCLX) is sufficient to trigger 'AD-like' pathology, including mitochondrial dysfunction, amyloid deposition and tau pathology, and cognitive decline. In addition, we found significant proteomic remodeling of components of the mitochondrial calcium uniporter channel (mtCU), the primary mediator of Ca uptake, in frontal cortex samples isolated post-mortem from patients diagnosed with non-familial/sporadic AD.
View Article and Find Full Text PDFDeveloping Topics.
Alzheimers Dement
December 2024
University of Kentucky College of Medicine, Sanders-Brown Center on Aging, Lexington, KY, USA.
Background: Astrocytes are a glial cell type responsible for many protective functions in the brain. While they are primarily recognized for regulating synaptic activity, they're also essential for maintaining the neurovascular unit, and cerebral hyperperfusion during metabolic demand. Calcium signaling has been identified as a regulatory process for these functions.
View Article and Find Full Text PDFDeveloping Topics.
Alzheimers Dement
December 2024
Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON, Canada.
Background: The relevance of a plasma membrane Na-Ca exchanger isoform-3 protein, NCX3, is widely evidenced in neuronal physiology. However, the mechanisms leading to NCX3 expression deficits in Alzheimer's disease (AD) pathology and its value as a target in AD pharmacological medicine remain incomplete.
Methods: Inhibition and rescue experiments were performed in cultured primary neurons of 5×FAD mice model of AD using pathological Aβ isolated from a conditioned medium of BHK cells, a cell line which does not constitutively express NCX3, stably transfected with a plasmid expressing human wild type Aβ.
Background: Understanding the fundamental differences between the human and pre-human brain is a prerequisite for designing meaningful models and therapies for AD. Expressed CHRFAM7A, a human restricted gene with carrier frequency of 75% in the human population predicts profound translational significance.
Method: The physiological role of CHRFAM7A in human brain is explored using multiomics approach on 600 post mortem human brain tissue samples (ROSMAP).
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