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Astrocytes occupy a vast area within the central nervous system (CNS). Despite their abundance, the functional role of astrocytes in vivo has only begun to be uncovered. Astrocytes were typically thought to be involved in pathophysiological states. However, recent studies have shown that astrocytes are actively involved in cell signaling in normal physiological states; manipulating various aspects of astrocytic cell signaling in vivo has revealed that astrocytes are key players in controlling healthy behavior in the absence of pathophysiology. Unfortunately, the study of astrocyte function is often limited by the number of approaches available due to our lack of understanding of cell physiology. This review summarizes recent studies in which altered astrocyte signaling capacity resulted in dramatic changes in behavior. We not only discuss the methodologies available to manipulate astrocytes but also provide insights into the behavioral roles of astrocytes in the CNS.
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http://dx.doi.org/10.1038/s12276-020-0468-z | DOI Listing |
Cell Mol Biol (Noisy-le-grand)
September 2025
Department of Hematology and Blood Banking, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Despite significant advancements in the treatment of non-small cell lung cancer (NSCLC) using conventional therapeutic methods, drug resistance remains a major factor contributing to disease recurrence. In this study, we aimed to explore the potential benefits of combining PI3K inhibition with Cisplatin in the context of NSCLC-derived A549 cells. Human non-small cell lung cancer A549 cells were cultured and treated with BKM120, cisplatin, or their combination.
View Article and Find Full Text PDFArch Pharm Res
September 2025
College of Pharmacy, Hanyang University, Ansan, 15588, Republic of Korea.
c-Jun N-terminal kinases (JNKs), a subfamily of mitogen-activated protein kinases (MAPKs), are key mediators of cellular responses to environmental stress, inflammation, and apoptotic signals. The three isoforms-JNK1, JNK2, and JNK3 exhibit both overlapping and isoform-specific functions. While JNK1 and JNK2 are broadly expressed across tissues and regulate immune signaling, cell proliferation, and apoptosis, JNK3 expression is largely restricted to the brain, heart, and testis, where it plays a crucial role in neuronal function and survival.
View Article and Find Full Text PDFMol Biol Rep
September 2025
Dr. B. R. Ambedkar Centre for Biomedical Research North Campus , University of Delhi, 110007, Delhi, India.
Background: Standard treatment for glioblastoma includes chemotherapy, alkylating agents such as temozolomide (TMZ); however, MGMT resistance leads to recurrence. Demethoxycurcumin (DMC) has been reported to inhibit cancer cell growth, induce apoptosis, and prevent metastasis in different cancer models. We investigated the DMC-induced apoptosis and autophagy via inhibition of the AKT/mTOR pathway in human glioma U87MG and T98G cell lines.
View Article and Find Full Text PDFMetab Brain Dis
September 2025
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Cairo, Egypt.
Acute or chronic liver damage can result in Hepatic Encephalopathy (HE), a potentially fatal neuropsychiatric condition that leads to cerebral and neurological alterations. Dapagliflozin (DAPA), an orally active Sodium/Glucose cotransporter 2 inhibitor with long duration of action. The study aim was to evaluate the potential protective impact of DAPA against HE caused by Thioacetamide (TAA) in rats.
View Article and Find Full Text PDFCell Mol Life Sci
September 2025
Department of Gastroenterology, The Second Hospital of Shandong University, Jinan, China.
Metabolic associated steatohepatitis (MASH) is a severe form of metabolic dysfunction-associated steatotic liver disease (MASLD) characterized by hepatocellular injury, inflammation, and fibrosis. Despite advances in understanding its pathophysiology, the molecular mechanisms driving MASH progression remain unclear. This study investigates the role of long non-coding RNA Linc01271 in MASLD/MASH pathogenesis, ant its involvement in the miR-149-3p/RAB35 axis and PI3K/AKT/mTOR signaling pathway.
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