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Inflammation is a necessary immunological response that promotes survival and preserves tissue homeostasis, a common characteristic linked to various diseases. However, in some circumstances, the inflammatory response is deleterious and contributes to disease pathogenesis. Anti-inflammatory substances have poor affinity for inflamed tissues, resulting in low concentrations in the target tissue and a higher incidence of severe adverse effects. To address this issue, several potential approaches have been proposed, such as chemical modification of drug molecules and the development of nanocarriers for drug delivery. Since the development of nanotechnology at the beginning of the twenty-first century, researchers have been using the pathophysiological characteristics of inflammation, primarily leaky vasculature, and biomarker overexpression to develop nanomedicines that can deliver therapeutics via passive and active targeting mechanisms to sites of inflammation and produce therapeutic effects. Drug carriers based on nanoparticles can enhance the safety and efficacy of drugs by increasing their capacity, enhancing their solubility, combining several drugs, protecting them from metabolism, and regulating their release. An approach that shows promise in the treatment of various inflammatory diseases is the application of nanomedicines. Nanomedicine involves nanoparticles that have been loaded with a therapeutically active component. Nanomedicines can target inflammation by recognizing molecules highly expressed on endothelial cells or activated macrophage surfaces, enhancing the permeability of vessels, or even by biomimicry. A review of the research findings shows significant potential for the use of nanotechnology to enhance the quality of life for people using NSAIDs for chronic disorders by minimizing drug side effects or the duration of administration. After a brief introduction to inflammation, its various forms- acute and chronic inflammation, and the pathophysiology of inflammation, this review highlights the main innovative nanocarriers utilized for carrying various nonsteroidal anti-inflammatory drugs that have been utilized in treating various inflammatory disorders.
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http://dx.doi.org/10.1007/s10787-025-01644-x | DOI Listing |
J Cereb Blood Flow Metab
September 2025
The Vivian L. Smith Department of Neurosurgery, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX, USA.
Aneurysmal subarachnoid hemorrhage (aSAH) is a devastating neurological disease, and one of the primary drivers of morbidity after aneurysm rupture is the phenomenon of delayed cerebral ischemia (DCI). Significant knowledge has been gained over the past two decades of the impact of neuroinflammation in DCI; and neutrophils are now believed to play a major role. There is significant human subject data showing the rise of neutrophil related inflammatory markers and neutrophil's association with poor outcome after aSAH, but as of yet no trials involving human subjects have been done specifically targeting neutrophils.
View Article and Find Full Text PDFCurr Opin Lipidol
August 2025
Cardiometabolic Immunity Laboratory, Department of Physiology, Monash Biomedicine Discovery Institute (BDI) and Victorian Heart Institute (VHI), Monash University, Melbourne, Victoria, Australia.
Purpose Of Review: This review explores the evolving understanding of efferocytosis - the clearance of dead or dying cells by phagocytes - in the context of atherosclerosis. It highlights recent discovers in cell death modalities, impaired clearance mechanisms and emerging therapeutic strategies aimed at restoring efferocytosis to stabilize plaques and resolve inflammation.
Recent Findings: Recent studies have expanded the scope of efferocytosis beyond apoptotic cells to include other pro-inflammatory cell death modes, including pyroptosis, necroptosis and ferroptosis, revealing context-dependent clearance efficiency and immunological outcomes.
Mult Scler
September 2025
Department of Quantitative Health Sciences, Mayo Clinic, Rochester, MN, USA.
Background: Tumefactive demyelination (TD) is a rare variant of multiple sclerosis (MS) characterized by tumor-like lesions that often require aggressive management. Genome-wide association studies (GWAS) identified variants associated with MS; similar analyses in TD are lacking.
Objective: A GWAS was performed to identify variants associated with TD.
Curr Opin Neurol
October 2025
Neuromuscular Diseases Unit, Department of Neurology, IR SANT PAU, Hospital de la Santa Creu i Sant Pau, CIBERER, Barcelona, Spain.
Purpose Of Review: Autoimmune nodopathies (AN) are a recognized distinct group of immune-mediated peripheral neuropathies with unique immunopathological features and therapeutic implications. This review synthesizes recent advances in their pathogenesis, diagnosis, and management, which have refined their clinical classification and informed targeted treatment strategies.
Recent Findings: AN are characterized by autoantibodies targeting surface proteins in the nodal-paranodal area (anti-contactin-1, anti-contactin-associated protein 1, anti-neurofascin-155, anti-pan-neurofascin), predominantly of IgG4 subclass.
Macrophage Migration Inhibitory Factor (MIF) is a pleiotropic cytokine that acts as a central regulator of inflammation and immune responses across diverse organ systems. Functioning upstream in immune activation cascades, MIF influences macrophage polarization, T and B cell differentiation, and cytokine expression through CD74, CXCR2/4/7, and downstream signaling via NF-κB, ERK1/2, and PI3K/AKT pathways. This review provides a comprehensive analysis of MIF's mechanistic functions under both physiological and pathological conditions, highlighting its dual role as a protective mediator during acute stress and as a pro-inflammatory amplifier in chronic disease.
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