Neurosteroids have a crucial role in physiological intrinsic regulations of the Central Nervous System functions. They are derived from peripheral steroidogenic sources and from the de novo neurosteroidogenic capacity of brain cells. Significant alterations of neurosteroid levels have been frequently observed in neuroinflammation and neurodegenerative diseases. Such level fluctuations may be useful for both diagnosis and treatment of these pathological conditions. Beyond steroid administration, enhancing the endogenous production by Translocator Protein (TSPO) targeting has been proposed to restore these altered pathological levels. However, the neurosteroid quantification and the prediction of their final effects are often troublesome, sometimes controversial and context dependent, due to the complexity of neurosteroid biosynthetic pathway and to the low produced amounts. The aim of this review is to report recent advances, and technical limitations, in neurosteroid-related strategies against neuroinflammation.
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http://dx.doi.org/10.1016/j.neuint.2024.105916 | DOI Listing |
FASEB J
January 2025
Department of Nutrition, Second Military Medical University, Shanghai, China.
Tamoxifen is an inhibitor of estrogen receptors and was originally developed for breast cancer therapy. Besides, tamoxifen is widely used for Cre-estrogen receptor-mediated conditional knockout in transgenic mice. However, we found that the 3-month feeding of 0.
View Article and Find Full Text PDFBiochem J
January 2025
University of Pittsburgh School of Medicine, Pittsburgh, United States.
The sodium phosphate cotransporter-2A (NPT2A) mediates basal and parathyroid hormone (PTH)- and fibroblast growth factor-23 (FGF23)-regulated phosphate transport in proximal tubule cells of the kidney. Both basal and hormone-sensitive transport require sodium hydrogen exchanger regulatory factor-1 (NHERF1), a scaffold protein with tandem PDZ domains, PDZ1 and PDZ2. NPT2A binds to PDZ1.
View Article and Find Full Text PDFCells
December 2024
Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, 37134 Verona, Italy.
Mutations in the genes , , and cause three clinically overlapping thrombocytopenias characterized by a predisposition to hematological neoplasms. The gene, which encodes a protein involved in protein-protein interactions, is downregulated by RUNX1 during megakaryopoiesis. Mutations in 5'UTR of ANKRD26, leading to ANKRD26-RT, disrupt this regulation, resulting in the persistent expression of ANKRD26, which leads to impaired platelet biogenesis and an increased risk of leukemia.
View Article and Find Full Text PDFCells
December 2024
Molecular and Cellular Microbiology Laboratory, Department of Biological Sciences, Old Dominion University, Norfolk, VA 23529, USA.
Within mammalian cells, diverse endocytic mechanisms, including phagocytosis, pinocytosis, and receptor-mediated endocytosis, serve as gateways exploited by many bacterial pathogens and toxins. Among these, caveolae-mediated endocytosis is characterized by lipid-rich caveolae and dimeric caveolin proteins. Caveolae are specialized microdomains on cell surfaces that impact cell signaling.
View Article and Find Full Text PDFEndocr Metab Immune Disord Drug Targets
January 2025
Department of Biochemistry, KVG Medical College and Hospital, Sullia 574327, India.
Type 2 Diabetes Mellitus (T2DM) is an etiologically diverse metabolic dysfunction that, if untreated, leads to chronic hyperglycemia. Understanding the etiology of T2DM is critical, as it represents one of the most formidable medical challenges of the twenty-first century. Traditionally, insulin resistance has been recognized as the primary risk factor and a well-known consequence of type 2 diabetes.
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