98%
921
2 minutes
20
Stroke is a life-threatening condition in which accurate diagnoses and timely treatment are critical for successful neurological recovery. The current acute treatment strategies, particularly non-invasive interventions, are limited, thus urging the need for novel therapeutical targets. Arginine vasopressin (AVP) receptor antagonists are emerging as potential targets to treat edema formation and subsequent elevation in intracranial pressure, both significant causes of mortality in acute stroke. Here, we summarize the current knowledge on the mechanisms leading to AVP hyperexcretion in acute stroke and the subsequent secondary neuropathological responses. Furthermore, we discuss the work supporting the predictive value of measuring copeptin, a surrogate marker of AVP in stroke patients, followed by a review of the experimental evidence suggesting AVP receptor antagonists in stroke therapy. As we highlight throughout the narrative, critical gaps in the literature exist and indicate the need for further research to understand better AVP mechanisms in stroke. Likewise, there are advantages and limitations in using copeptin as a prognostic tool, and the translation of findings from experimental animal models to clinical settings has its challenges. Still, monitoring AVP levels and using AVP receptor antagonists as an add-on therapeutic intervention are potential promises in clinical applications to alleviate stroke neurological consequences.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9916514 | PMC |
http://dx.doi.org/10.3390/ijms24032119 | DOI Listing |
Med Lett Drugs Ther
September 2025
Zhonghua Jie He He Hu Xi Za Zhi
September 2025
Department of nursing, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou 510000, China.
Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKI) are important treatments for EGFR mutant non-small cell lung cancer (NSCLC). However, the first and second generation EGFR-TKI face clinical limitations due to acquired resistance, such as the T790M mutation. Irreversible EGFR-TKI can significantly prolong the survival of patients by enhancing the inhibition of drug-resistant mutations through the covalent binding mechanism.
View Article and Find Full Text PDFRedox Biol
August 2025
Department of Medicine, School of Medicine, Universidad Autónoma de Madrid, Madrid, Spain; Instituto Investigación Sanitaria-Princesa IIS-IP, Madrid, Spain; Centro de Investigación Biomédica en Red de Enfermedades Respiratorias (CIBERES), Instituto de Salud Carlos III, Madrid, Spain. Electronic
Tobacco smoke is the main risk factor for the development of chronic obstructive pulmonary disease (COPD). Despite current therapies alleviate symptoms there are limitations in the efficacy of treatments to curb its cardiovascular morbidities, particularly vascular dysfunction and the development of pulmonary hypertension. Our previous studies demonstrate that cigarette smoke directly contributes to pulmonary arterial dysfunction.
View Article and Find Full Text PDFJ Neurophysiol
September 2025
Department of Neurosurgery, University of Utah School of Medicine, Salt Lake City, UT, USA.
Although glutamatergic and GABAergic synapses are important in seizure generation, the contribution of non-synaptic ionic and electrical mechanisms to synchronization of seizure-prone hippocampal neurons remains unclear. Here, we developed a physiologically relevant model to study these mechanisms by inducing prolonged seizure-like discharges (SLDs) in hippocampal slices from male rats through modest, sustained ionic manipulations. Specifically, we reduced extracellular calcium to 0.
View Article and Find Full Text PDFNeuropsychobiology
September 2025
Introduction: Anxiety has been described in the initial stages of schizophrenia, and affective flattening in the chronic illness. The etiology remains unknown. Ketamine, a noncompetitive N-Methyl-D-amino-aspartate acid (NMDA) receptor antagonist, is used in rats as a translational model of schizophrenia.
View Article and Find Full Text PDF